最新刊期
卷 32 ， 期 12 ， 2026
- 摘要：ObjectiveThis paper aims to evaluate the pharmacological effect of Shenling Baizhusan with Codonopsis Radix as a monarch drug on improving the emotional state of rats with diarrhea-predominant irritable bowel syndrome （IBS-D） and explore its potential mechanism of action.Methods48 1-day-old SPF-grade male suckling rats were divided into six groups： blank group， model group， Shenling Baizhusan group （10.08 g·kg-1·d-1）， Shenling Baizhusan group without Codonopsis Radix （8.73 g·kg-1·d-1）， Codonopsis Radix group （1.35 g·kg-1·d-1）， and pinaverium bromide group （0.013 5 g·kg-1·d-1）， with eight rats per group. Except for those in the blank group， rats in other groups received maternal separation， senna leaf granule gavage， and chronic unpredictable stress to establish a rat model with IBS-D. Drug administration was initiated when the rats were eight weeks old for two consecutive weeks of intervention. The body weight of rats in all groups was recorded to observe body weight gain. The diarrhea status was evaluated by the Bristol stool scale score and fecal water content. Abdominal pain was assessed via the abdominal withdrawal reflex （AWR）. Anxiety- and depression-like emotional states were evaluated by using the open field test （OFT）， forced swimming test （FST）， and sucrose preference test （SPT）. Western blot was used to detect the protein expression levels of tight junction proteins Claudin1 and Occludin， as well as zonula occludens-1 （ZO-1） in the colonic tissues of rats. Meanwhile， it was also used to determine the expression levels of glial fibrillary acidic protein （GFAP）， ionized calcium-binding adapter molecule 1 （IBA1）， and Synapsin1 in the hippocampal tissues of rats in all groups. Enzyme linked immunosorbent assay （ELISA） was employed to measure tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in the serum， as well as the content of brain-derived neurotrophic factor （BDNF） in the hippocampal tissues of rats in all groups.ResultsCompared with those in the blank group， the rats in model group showed slow body weight gain with lower body weight （P<0.01）， increased Bristol stool scale scores （P<0.01）， higher fecal water content （P<0.01）， and elevated AWR scores （P<0.05）. In contrast to those in blank group， Shenling Baizhusan with Codonopsis Radix as monarch drug significantly improved the slow body weight gain （P<0.01）， reduced Bristol stool scale scores （P<0.01） and fecal water content （P<0.01）， as well as decreased visceral sensitivity （P<0.01）， exhibiting the optimal therapeutic effect among the drugs in all the groups. Behavioral test results reveal that， compared with those in the blank group， rats in the model group have a shorter total movement distance （P<0.01）， fewer movement counts （P<0.01）， shorter movement duration （P<0.01）， longer immobility time （P<0.01）， and lower sucrose preference （P<0.01）. After drug intervention， Shenling Baizhusan with Codonopsis Radix as monarch drug demonstrated the best intervention effect， and it significantly increased the total movement distance （P<0.01）， movement counts （P<0.01）， and movement duration （P<0.01）， while decreasing immobility time （P<0.01） and increasing sucrose preference （P<0.01） in the treated rats. Western blot analysis indicates that， compared with those in blank group， rats in model group have significantly downregulated expression levels of tight junction proteins Claudin1， Occludin and ZO-1 in colonic tissues （P<0.01）， as well as Synapsin1 in hippocampal tissues （P<0.01）， along with significantly upregulated expression levels of GFAP and IBA1 in hippocampal tissues （P<0.01）. After intervention with Shenling Baizhusan with Codonopsis Radix as the monarch drug， the expression levels of tight junction proteins in colonic tissues and Synapsin1 in hippocampal tissues were significantly increased （P<0.01）， while the expression levels of GFAP and IBA1 were significantly decreased （P<0.01）. ELISA results show that， compared with those in the blank group， rats in the model group have higher contents of TNF-α and IL-6 （P<0.01） in serum and a significantly lower BDNF level in hippocampal tissues （P<0.01）. After intervention with Shenling Baizhusan with Codonopsis Radix as the monarch drug， the contents of TNF-α and IL-6 were reduced （P<0.01）， and the content of BDNF in hippocampal tissues was increased.ConclusionShenling Baizhusan with Codonopsis Radix as the monarch drug plays a role in improving abdominal pain， diarrhea， as well as anxiety- and depression-like behaviors in rats with IBS-D. Its potential mechanism of action may exert therapeutic effects by repairing the damaged intestinal mucosal barrier， alleviating low-grade inflammatory responses， and inhibiting the excessive activation of central glial cells.关键词：Shenling Baizhusan;Codonopsis Radix;irritable bowel syndrome;emotion;nerve cell269|129|0更新时间：2026-05-15
- 摘要：ObjectiveTo investigate the mechanism by which Guipitang regulates mitochondrial biogenesis of hippocampal neurons in methylmalonic aciduria （MMA） rats through the adenosine monophosphate-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1α （AMPK/PGC-1α） signaling pathway.MethodsFifty 5-day-old Wistar rats were randomly divided into a blank group， a model group， a Guipitang group （9.3 g·kg-1）， an AMPK inhibitor group （2.5 mg·kg-1 Compound C）， and a Guipitang + AMPK inhibitor group （9.3 g·kg-1 + 2.5 mg·kg-1 Compound C） using a random number table method. After 3 weeks of administration， the Morris water maze test was used to assess the rats' learning and memory abilities. Hematoxylin-eosin （HE）， Nissl， and terminal deoxynucleotidyl transferase dUTP nick end labeling （TUNEL） staining was performed to detect histopathological changes and apoptosis in rat hippocampal tissue. Colorimetric assays were employed to measure mitochondrial adenosine triphosphate （ATP） content in hippocampal tissue. The mitochondrial superoxide red fluorescent probe method （MitoSOX Red） was used to assess mitochondrial reactive oxygen species （ROS） levels. The JC-1 assay was carried out to detect mitochondrial membrane potential in hippocampal tissue. Transmission electron microscopy （TEM） was conducted to observe pathological changes in mitochondria. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect mitochondrial DNA copy numbers. Western blot was employed to detect AMPK， PGC-1α， phosphorylated AMPK （p-AMPK）， nuclear factor E2-related factor 1 （Nrf1）， nuclear factor E2-related factor 2 （Nrf2）， and mitochondrial transcription factor A （TFAM） in rat hippocampal tissue.ResultsCompared with those in the blank group， rats in the model group exhibited more dispersed movement paths， were unable to locate the platform independently， and had prolonged escape latency， reduced frequency of crossing the platform， significantly reduced time spent in the target quadrant， and significantly increased time spent in the opposite quadrant （P<0.01）. Compared with those in the model group， rats in the Guipitang group and the Guipitang + AMPK inhibitor group had significantly shortened escape latency， significantly increased frequency of crossing the platform， significantly increased time spent in the target quadrant， and significantly reduced time spent in the opposite quadrant （P<0.05， P<0.01）. Compared with the Guipitang group， the AMPK inhibitor group had a longer escape latency， significantly reduced frequency of crossing the platform， significantly reduced time spent in the target quadrant， and significantly increased time spent in the opposite quadrant （P<0.01）. The model group showed disorganized arrangement of hippocampal neurons and nuclear pyknosis. After treatment with Guipitang， the number of regular neurons increased， while the improvement in the Guipitang + AMPK inhibitor group was less than that in the Guipitang group （P<0.01）. Electron microscopy showed that the cristae structure of mitochondria was extensively lost in the model group， but significantly recovered in the Guipitang group （P<0.01）. The Guipitang + AMPK inhibitor group still exhibited mitochondrial membrane rupture and reduced cristae structure. The apoptosis rate was significantly increased in the model group. Compared with the blank group， the model group had significantly increased ROS levels， significantly reduced ATP content， and significantly decreased mitochondrial membrane potential （P<0.01）. Compared with the model group， the Guipitang group had significantly reduced ROS levels， significantly increased ATP content， and significantly increased mitochondrial membrane potential （P<0.01）. Compared with the model group， the Guipitang group showed a significant decrease in apoptosis rate （P<0.01）， and this effect was partially reversed by the AMPK inhibitor （P<0.01）. The model group showed significantly reduced TFAM， PGC-1α， Nrf1， and Nrf2 mRNA expression and protein expression levels （P<0.01）. Compared with the model group， the Guipitang group showed significantly increased TFAM， PGC-1α， Nrf1， and Nrf2 mRNA expression and protein expression levels （P<0.01）. Compared with the blank group， the model group showed significantly reduced p-AMPK/AMPK protein expression levels （P<0.01）. Compared with the model group， the Guipitang group showed significantly increased p-AMPK/AMPK protein expression levels （P<0.01）.ConclusionGuipitang can improve cognitive dysfunction in rats by activating the AMPK/PGC-1α signaling pathway， promoting mitochondrial biogenesis， and alleviating pathological damage to hippocampal neurons.关键词：Guipitang;methylmalonic aciduria （MMA）;mitochondrial biogenesis;adenosine monophosphate-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1α （AMPK/PGC-1α） signaling pathway360|191|0更新时间：2026-05-15
- 摘要：Cancer-related anxiety and depression are common pathological emotional changes in patients with cancer and seriously affect quality of life and disease prognosis. Current cancer treatment focuses mainly on anti-tumor efficacy while neglecting patients emotional problems during diagnosis and treatment. In addition， functional decline and social dysfunction at different stages of cancer may lead to the occurrence of anxiety and depression， reduce treatment adherence， promote tumor infiltration and metastasis， and form a vicious cycle. Traditional Chinese medicine （TCM） has demonstrated definite efficacy in the treatment of cancer-related anxiety and depression. However， systematic clarification of anxiety and depression across the entire cancer process remains insufficient. The "five-phase evolution" theory， proposed by Professor LI Jie based on the academic concept of disease-syndrome integration， was summarized according to the physiological and pathological characteristics at different stages of tumor development. Its core connotation is the "five-phase evolution of deficiency-cold-toxin-closure-decline， with depression running throughout， and tumor toxin as the core". The pathogenesis of tumor-related anxiety and depression centers on "depression". This theory provides an innovative approach for the whole-course syndrome differentiation and treatment of cancer-related anxiety and depression. According to the clinical manifestations of patients at each stage and anti-tumor treatment， therapy emphasizes relieving depression as the main principle， focusing on regulating qi movement， and implementing stage-specific interventions based on the evolutionary characteristics of deficiency-cold-toxin-closure-decline. In the early stage of cancer， Qi-tonifying methods are applied as adjunctive treatment. During the perioperative period and radiochemotherapy， warming-yang methods are combined. In the disease progression stage， blood-activating and toxin-removing methods are used concurrently. In the middle and late stages， deficiency-tonifying and closure-unblocking therapies are combined. Meanwhile， "tumor toxin" is regarded as the core pathogenesis of cancer throughout the entire treatment process. Through dynamic syndrome differentiation， a diagnostic and therapeutic system of "relieving depression and combating cancer， with stage-based treatment" is constructed， providing new therapeutic ideas for TCM in the management of cancer-related anxiety and depression and guiding clinical practice.关键词：neoplasms;cancer-related anxiety;cancer-related depression;five-phase evolution;depression190|124|0更新时间：2026-05-15
- 摘要：Non-small cell lung cancer （NSCLC） is a clinically common malignant tumor. In recent years， immune checkpoint inhibitors （ICIs） have become a core treatment modality in the perioperative period and for advanced diseases. However， drug resistance and immune-related adverse events （irAEs） remain critical bottlenecks limiting long-term patient benefits. Currently， modern medicine lacks systematic intervention strategies， and an integrated treatment system combining traditional Chinese and Western medicine for immunotherapy has yet to be established. This study is grounded in the theory of distance of lung fire from Wai Jing Wei Yan， employing the transmission and transformation of Qi-fire in five Zang-organs to elucidate the dynamic pathogenesis at various stages of NSCLC immunotherapy. The core pathogenesis of NSCLC can be categorized into two fundamental states： Distant fire （characterized by cold coagulation and Qi depletion） and near fire （characterized by intense heat scorching and Qi consumption）. Distant fire refers to the failure of Fire from other organs to reach the lung， leading to loss of warmth， congealing cold， and Qi depletion， manifesting as an initial immunosuppressed state. Specifically， the neoadjuvant therapy， adjuvant therapy， and advanced stages pertain to lung deficiency and Qi weakness， collapse of pectoral Qi and middle Qi， and decline of the life-gate fire， respectively. Near fire refers to pathogenic fire from other organs ascending to harass and scorch the lung， and intense fire consumes Qi， forming the pathogenic basis for irAEs. Specifically， the neoadjuvant therapy， adjuvant therapy， and advanced stages are attributed to lung fire-toxin accumulation， upsurge of Yin fire， and kidney deficiency with floating fire， respectively. Within each stage， a tendency toward drug resistance is attributed to constrained pivot of the liver， congealing into distant fire. However， this can also transform back into near fire， promoting disease progression. Furthermore， the prosperity or decline of the sovereign fire is related to the lung's governance and regulation， and is closely associated with initial immunosuppression， drug resistance， and irAEs. On this basis， our team proposes the core therapeutic principle of harmonizing the Qi-fire in five Zang-organs to restore the gentle warming of the subtle fire within the lung. For the transformation of distant fire， the treatment at neoadjuvant therapy， adjuvant therapy， and advanced stages focuses on regulating Qi-fire in the lung， fortifying the earth to generate metal， and reinforcing the root and cultivating the source， respectively. For the harm of near fire， the treatment at neoadjuvant therapy， adjuvant therapy， and advanced stages necessitates securing and protecting the lung， raising Yang and constraining Fire， and directing fire downward and anchoring the lung， respectively. In the drug-resistant progression phase， unblocking the pivot and expelling toxins can be used to improve immune status， while clearing lung and pacifying wood can be adopted to alleviate physical and mental symptoms. Additionally， on the basis of stage- and phase-specific syndrome differentiation， the treatment should regulate the sovereign fire from the heart， calming the spirit and harmonizing the mind. These methods are implemented concurrently without conflict， aiming to re-establish the body's state of Yin-Yang self-harmony， thereby providing a precise and dynamic theoretical basis and a clinical paradigm for integrated traditional Chinese medicine and immunotherapy for NSCLC.关键词：non-small cell lung cancer;distant fire;near fire;Qi-fire in five Zang-Organs;immune checkpoint inhibitor112|36|0更新时间：2026-05-15
- 摘要：ObjectiveTo investigate the inhibitory effects of Resina Draconis on Lewis lung carcinoma （LLC） in mice， elucidate its regulatory mechanisms on the tumor immune microenvironment， and evaluate its potential to sensitize tumors to anti-programmed death-1 antibody （αPD-1）.MethodsC57BL/6J mice weighing 18-20 g were subcutaneously inoculated with LLC cells to establish tumor-bearing mouse models. The model mice were randomly assigned into three groups （n=6 per group）： the model group， the low-dose （200 mg·kg-¹） Resina Draconis group， and the high-dose （400 mg·kg-¹） Resina Draconis group， and administrated with corresponding drugs for 14 consecutive days. Hematoxylin-eosin （HE） staining， immunohistochemistry， Real-time PCR， and flow cytometry were employed to assess antitumor efficacy and immunomodulation mechanism of Resina Draconis. In a subsequent combination therapy experiment， mice were allocated into control， Resina Draconis， αPD-1， and Resina Draconis + αPD-1 groups to evaluate the synergistic antitumor effects.ResultsCompared with the model group， high-dose Resina Draconis inhibited tumor growth （P<0.01）， achieving a tumor inhibition rate of 25.46%， which was higher than that （12.56%） of the low-dose group （P<0.05）. Compared with the model group， the high-dose Resina Draconis group showed pronounced pathological alterations in the tumor tissue， accompanied by increased cellular necrosis and apoptosis. Moreover， high-dose Resina Draconis promoted the maturation of dendritic cells （DCs） within the tumor microenvironment （P<0.01）， increased the infiltration of cytotoxic T lymphocytes （CTLs） （P<0.05）， elevated effector CTL levels （P<0.05）， and enhanced helper T-cell infiltration （P<0.05）. In addition， it enhanced the functional activity of CTLs， as evidenced by the upregulated mRNA levels of interferon-γ （IFN-γ） and tumor necrosis factor-α （TNF-α） （P<0.01）. Macrophage infiltration was also significantly increased （P<0.01）， promoting the polarization toward anti-tumor M1 macrophages. In addition， high-dose Resina Draconis increased the proportions of DCs and CTLs in the spleen （P<0.01） and enhanced the differentiation of effector CTLs compared with the model group. The combination therapy experiment showed that compared with αPD-1 alone， Resina Draconis + αPD-1 exhibited enhanced antitumor effects， with the tumor inhibition rate increasing from 31.86% to 42.55% （P<0.05）.ConclusionResina Draconis exerts antitumor effects in LLC-bearing mice by modulating key immune cell populations， including DCs， T cells， and macrophages， thereby enhancing their infiltration and functional activation. This remodeling of the tumor immune microenvironment strengthens local antitumor immunity and activates systemic immune responses， ultimately suppressing tumor growth. Furthermore， Resina Draconis synergistically enhances the efficacy of αPD-1， demonstrating the potential as an adjuvant strategy to improve immune checkpoint therapy.关键词：Resina Draconis;lung cancer;tumor microenvironment;immunomodulation;anti-programmed death-1 antibody （αPD-1）109|33|0更新时间：2026-05-15
- 摘要：ObjectiveTo establish an animal model of postoperative respiratory dysfunction in lung cancer with Qi sinking syndrome， thereby providing an ideal tool for related research and exploring the rehabilitation-promoting effects and mechanisms of Shengxian Qingjin decoction （SXQJ）.MethodsLewis-luc lung cancer cells at varying concentrations were injected intrapulmonary to establish an orthotopic lung tumor model in mice. Tumor growth was monitored via micro-CT， in vivo bioluminescence imaging， and hematoxylin-eosin （HE） staining. Under ventilator support， left lobectomy was performed to create a postoperative respiratory dysfunction model with Qi sinking syndrome. Mice were assigned into normal， model， and SXQJ （14.95 g·kg-1·d-1） groups. The intervention lasted for 14 days. Four time points were established on postoperative day 0， 5， 10， 15 for dynamic observation. Pulmonary function tests， lung HE staining， and pathological analysis were performed to elucidate changes in respiratory dysfunction after lung cancer surgery. Symptoms scores， neogenic hair growth in the surgical area， and tongue coating were assessed to evaluate alterations in the Qi sinking syndrome. Exercise endurance and open field tests were conducted to assess changes in the functional status of the model mice. Immunofluorescence staining was adopted to detect podoplanin （PDPN） to evaluate the level of alveolar epithelial type Ⅰ cells （AT1）， and surfactant protein C （SFTPC） and nuclear associated antigen （Ki67） were employed to evaluate the proliferation level of alveolar epithelial type Ⅱ cells （AT2）. Western blot was used to measure the expression levels of proteins in the Wnt signaling pathway.ResultsThe high-concentration Lewis-luc group established faster progression of orthotopic lung cancer than the low-concentration group. The low-dose group reached lung cancer stages T1， T2， and T3 on day 3， 6， 9， respectively， while the high-dose group reached T4 on day 9. An animal model of postoperative respiratory dysfunction and Qi sinking syndrome following stage Ⅰ lung cancer surgery was successfully established. Compared with the normal group， the model group exhibited a decrease in body weight （P<0.05） and a decline in pulmonary function， manifested as increased inspiratory time， expiratory time， respiratory interval， minimal respiratory work， airway resistance， and elastic resistance， along with decreased tidal volume， expiratory volume， respiratory frequency， deep inspiratory capacity， and compliance （P<0.05）. In addition， the model group exhibited increased mean alveolar area and mean linear intercept and reduced lung parenchymal area （P<0.05）. The main symptom cluster in the model mice included shortness of breath， aversion to wind and cold， fatigue， dull and brittle fur， reduced food intake， constipation， and dry tongue coating with reduced moisture， consistent with the characteristics of Qi sinking syndrome. The hair in the surgical area showed slow regeneration， coarse texture， and reduced diameter （P<0.01）. Furthermore， the model mice showed decreased exercise endurance and total distance traveled in the open field test （P<0.05）， reduced expression of PDPN in the lung tissue （P<0.01）， increased proliferation of AT2 cells on postoperative day 10 （P<0.05）， and decreased expression of Wnt family members 3a （Wnt3a）， Wnt7a， and β-catenin （P<0.01）. Compared with the model group， the SXQJ group showed an increase in deep inspiratory capacity and a reduction in minimal respiratory work （P<0.05）， decreased mean alveolar area and mean linear intercept， and increased lung parenchymal area （P<0.05）. In addition， the SXQJ group showed alleviation of symptoms and improved tongue coating， along with enhanced quality and diameter of newly grown hair （P<0.05） and increased exercise endurance （P<0.05）， though the total distance traveled in the open field test did not show a statistically significant increase （P>0.05）. Furthermore， this group exhibited elevated expression of PDPN+AT1 in the lung tissue and increased SFTPC+Ki67+AT2 from postoperative days 5 to 15 （P<0.05） and upregulated protein levels of Wnt3a， Wnt7a， and β-catenin （P<0.05）.ConclusionAn animal model of postoperative respiratory dysfunction with Qi sinking syndrom after lung cancer surgery was successfully established. SXQJ demonstrated rehabilitation-promoting effects by regulating the Wnt/β-catenin signaling pathway， promoting AT2 cell proliferation and differentiation， and enhancing repair efficiency.关键词：after lung cancer surgery;respiratory dysfunction;Qi sinking syndrome;animal model establishment;Shengxian Qingjin decoction;rehabilitation112|85|0更新时间：2026-05-15
- 摘要：ObjectiveTo investigate the improvement effect and mechanism of Danlianxin formula （DLXF） on cardiac function associated with myocardial infarction （MI） in hyperlipidemic rats.MethodsThe hyperlipidemia model was established by feeding rats a high-fat diet for 8 weeks， followed by the MI modeling induced by ligating the left anterior descending coronary artery. After 4 weeks of gavage administration of DLXF at low （1.108 g·kg-1·d-1） and high （2.217 g·kg-1·d-1） doses， the following assessments were conducted： Observation of physical signs， echocardiography for cardiac function， histopathological examination for cardiac morphology， laser speckle contrast imaging for mesenteric microvascular perfusion， serum biochemical tests for key lipid parameters such as total cholesterol （TC） and triglycerides （TG）， as well as inflammatory cytokines including interleukin-1β （IL-1β）， IL-6， N-terminal pro-brain natriuretic peptide （NT-proBNP）， and tumor necrosis factor-α （TNF-α）， and Real-time PCR and Western blot analysis for the expression of cAMP-regulated guanine nucleotide exchange factor 1 （Epac1）， voltage-dependent anion channel 1 （VDAC1）， NOD-like receptor thermal protein domain associated protein 3 （NLRP3）， cysteinyl aspartate-specific proteinase （Caspase）-9， and Caspase-3.ResultsThe survival status of rats was generally improved in the DLXF group. Echocardiography revealed that compared with the model group， the high-dose DLXF group exhibited increased left ventricular ejection fraction （LVEF） and left ventricular short-axis shortening fraction （LVFS）， while both DLXF groups showed reduced left ventricular internal diameter at end-diastole （LVIDd） and left ventricular internal diameter at end-systole （LVIDs） （P<0.01）. Dynamic laser speckle flow imaging revealed reduced blood flow in the hyperlipidemia model group compared with the normal group （P<0.05）. Compared with that in the model group， mesenteric blood flow was increased in all drug treatment groups （P<0.01）. Serum biochemical test results showed that compared with those in the model group， both TC and TG levels were decreased in the low-dose DLXF group （P<0.05）， and the TG level was decreased in the high-dose group （P<0.05）. Both DLXF groups showed elevated high-density lipoprotein cholesterol （HDL-C） levels （P<0.05， P<0.01） and declined very low-density lipoprotein （VLDL） levels （P<0.01）， and the high-dose DLXF group exhibited a decreased low-density lipoprotein cholesterol （LDL-C） level （P<0.01）. enzyme-linked immunosorbent assay （ELISA） results showed that compared with those in the normal group， the IL-1β， IL-6， TNF-α， and NT-proBNP levels were elevated in the hyperlipidemia model group （P<0.01）. Compared with the model group， both DLXF groups showed a declining trend in serum IL-1β， IL-6， and TNF-α levels （P<0.05， P<0.01） and reduced NT-proBNP levels （P<0.01）. Histopathological findings revealed improved myocardial structure， regular fiber arrangement， reduced inflammatory infiltration， and diminished collagen proliferation in DLXF groups compared with the model group. Ultrastructural analysis of mitochondria demonstrated well-organized myocardial cell structure， orderly myofibrillar arrangement， and improved mitochondrial alignment with clear structure in DLXF groups compared with the model group. Myocardial cell apoptosis analysis revealed disordered cell arrangement and scattered brown apoptotic cells in the hyperlipidemia model group， with a higher number of apoptotic cells than the sham operation group. Compared with the model group， DLXF groups exhibited scattered apoptosis of varying degrees， altered cell morphology， and reduced apoptosis. Real-time PCR and Western blot results indicated that compared with the model group， DLXF downregulated the protein and mRNA levels of Epac1， VDAC1， NLRP3， Caspase-9， and Caspase-3 （P<0.05， P<0.01）.ConclusionDLXF can modulate the Epac1/VDAC1/NLRP3/Caspase signaling pathway to improve the mitochondrial structure and function and suppress inflammation， thereby enhancing cardiac function in myocardial infarction （MI） in hyperlipidemic rats.关键词：Danlianxin Formula;myocardial infarction;hyperlipidemia;mitochondria;energy metabolism645|82|0更新时间：2026-05-15
- 摘要：ObjectiveTo investigate the ameliorative effect of Jiangtang Xiaozhi tablets （JTXZT） on metabolic dysfunction-associated fatty liver disease， and to explore its mechanism from the perspectives of gut microbiota and hepatic bile acid synthesis.MethodsThirty healthy SPF C57BL/6J mice were randomly divided into a normal group， a model group， a high-dose JTXZT group （12.5 g·kg-1）， a low-dose JTXZT group （6.25 g·kg-1）， and an orlistat group （70 mg·kg-1）. The normal group was fed with normal diet， while the other groups were fed with high-fat diet for 12 weeks. Administration began in the fifth week， with gavage lasting for 8 weeks. Body composition， body weight， and liver weight were measured. Oral glucose tolerance test （OGTT） was conducted. Biochemical methods were used to detect the levels of triglycerides （TG）， total cholesterol （TC）， total bile acid （TBA）， alanine aminotransferase （ALT）， and aspartate aminotransferase （AST） in mice. Enzyme-linked immunosorbent assay （ELISA） was used to measure the levels of insulin， glucose， tumor necrosis factor-α （TNF-α）， and interleukin-6 （IL-6）. The insulin resistance index （HOMA-IR） was calculated. Hematoxylin-eosin （HE） staining was used to observe the pathological morphology of the liver， and oil red O staining was used to observe lipid deposition in the liver. High-throughput sequencing of 16S rRNA was used to detect changes in the gut microbiota of mice. Western blot and immunohistochemistry were used to detect changes in the protein expression levels of bile acid synthesis genes， cholesterol 7α-hydroxylase （CYP7A1） and farnesoid X receptor （FXR）.ResultsCompared with the normal group， the model group showed significantly increased body weight， liver weight， fat content， blood glucose levels at various time points after oral glucose administration and area under the curve （AUC）， insulin content， HOMA-IR， TG， TC， ALT， AST， TNF-α， and IL-6 levels （P<0.01） and a significantly decreased TBA level （P<0.05）. Pathological examination revealed steatosis and lipid accumulation in liver tissue， reduced diversity of gut microbiota communities， significantly decreased CYP7A1 protein expression （P<0.05， P<0.01）， and significantly increased FXR protein expression （P<0.01）. Compared with the model group， each treatment group showed significantly decreased body weight， liver weight， fat content， blood glucose levels at various time points after oral glucose administration and AUC， insulin content， HOMA-IR， TG， TC， ALT， AST， TNF-α， and IL-6 levels and a significantly increased TBA level （P<0.05， P<0.01）. Pathological examination showed significant improvement in steatosis and lipid accumulation in liver tissue， restoration of gut microbiota community diversity， changes in community composition， significantly increased CYP7A1 protein expression， and significantly decreased FXR protein expression （P<0.05， P<0.01）.ConclusionJTXZT can improve liver steatosis in mice with metabolic dysfunction-associated fatty liver disease， alleviate insulin resistance and inflammatory damage， and promote bile acid synthesis by regulating the diversity and structure of gut microbiota， thereby achieving the therapeutic effect on metabolic dysfunction-associated fatty liver disease.关键词：Jiangtang Xiaozhi tablets;metabolic dysfunction-associated fatty liver disease;gut microbiota;bile acid synthesis104|42|0更新时间：2026-05-15
- 摘要：ObjectiveTo investigate the protective effects and molecular mechanisms of the Sargassum-Glycyrrhizae Radix et Rhizoma incompatible herb pair within modified Haizao Yuhutang （HYT） on the liver of goiter model rats.MethodsA total of 128 male Wistar rats were randomly divided into eight groups （n=16 per group）： blank group， model group， Euthyrox group （20 μg·kg-1）， HYT group （12.06 g·kg-1）， HYT-H group （de-Sargassum， 9.90 g·kg-1）， HYT-G group （de-Glycyrrhizae， 10.26 g·kg-1）， HYT-HG group （de-Sargassum and de-Glycyrrhizae， 8.10 g·kg-1）， and HG group （3.96 g·kg-1）. Except for the blank group， all rats were administered propylthiouracil （PTU） by gavage for 14 consecutive days to establish a goiter model， followed by 14 days of corresponding drug intervention. Levothyroxine sodium tablets （Euthyrox） were used as the positive control. The blank group received deionized water by gavage. Serum levels of aspartate aminotransferase （AST） and alanine aminotransferase （ALT） were measured. Levels of reactive oxygen species （ROS）， malondialdehyde （MDA）， glutathione （GSH）， and oxidized glutathione （GSSG） in liver tissue were determined. Hematoxylin-eosin （HE） staining was used to observe histopathological changes in the liver， and transmission electron microscopy （TEM） was used to examine hepatocyte ultrastructure. Western blot was performed to detect the expression of adenosine monophosphate-activated protein kinase （AMPK）， phosphorylated AMPK （p-AMPK）， mammalian target of rapamycin （mTOR）， phosphorylated mTOR （p-mTOR）， UNC-51-like kinase 1 （ULK1）， and phosphorylated ULK1 （p-ULK1） in liver tissue.ResultsCompared with the blank group， the model group showed significantly increased serum AST and ALT levels （P<0.01）， a significantly decreased GSH/GSSG ratio in liver tissue （P<0.01）， significantly increased ROS and MDA levels （P<0.01）， and a significantly decreased p-ULK1/ULK1 ratio （P<0.05）. Compared with the model group， the HYT group showed significantly decreased serum AST and ALT levels （P<0.05， P<0.01）， a significantly increased GSH/GSSG ratio in liver tissue （P<0.01）， and significantly decreased ROS and MDA levels （P<0.01）. HE staining and TEM showed that liver morphology tended to return toward normal. In addition， the p-AMPK/AMPK ratio was significantly increased （P<0.05）， the p-mTOR/mTOR ratio was significantly decreased （P<0.01）， and the p-ULK1/ULK1 ratio was significantly increased （P<0.01）.ConclusionHYT containing Sargassum and Glycyrrhizae Radix et Rhizoma exerts protective effects on the liver of goiter model rats， with superior efficacy compared with the component-deleted and HG groups. Its mechanisms may be related to activation of the AMPK/mTOR/ULK1 signaling pathway， thereby inducing autophagy， promoting the clearance of damaged organelles and oxidative products， inhibiting ROS and MDA production， and restoring redox homeostasis.关键词：Haizao Yuhutang;Sargassum-Glycyrrhizae Radix et Rhizoma incompatible pair;goiter;oxidative stress in the liver;adenosine monophosphate-activated protein kinase （AMPK）/mammalian target of rapamycin （mTOR）/UNC-51-like kinase 1 （ULK1） signaling pathway98|40|0更新时间：2026-05-15
- 摘要：ObjectiveThis paper aims to investigate the protective mechanism of Liangxue Tuizi prescription on renal injury in immunoglobulin A （IgA） vasculitis （IgAV） model rats via toll‑like receptor 4 （TLR4）/nuclear transcription factor-κB （NF-κB）/NOD‑like receptor pyrin domain‑containing 3 （NLRP3） pathway-mediated oxidative stress.MethodsA total of fifty four-week-old male Wistar rats were randomly divided into a blank group with 10 rats and a modeling group with 40 rats. An IgAV rat model with renal injury was established by using a modified ovalbumin combined with a blood-heat syndrome method. Thirty successfully modeled rats were then randomly divided into the following six groups： the IgAV model group， the low-dose Liangxue Tuizi prescription group （3.75 g·kg-1）， the medium-dose Liangxue Tuizi prescription group （7.5 g·kg-1）， the high-dose Liangxue Tuizi prescription group （15 g·kg-1）， the TLR4 inhibitor group （3 mg·kg-1）， and the blank group， with six rats per group. The rats in all groups received drug interventions for four weeks. The general conditions of the rats， including mental status， behavior， and skin rash， were observed. The 24-hour urinary protein quantification and urinary red blood cell levels were measured. The levels of malondialdehyde （MDA）， reduced glutathione （GSH）， interleukin-18 （IL-18）， and intercellular adhesion molecule-1 （ICAM-1） in serum were detected by using enzyme linked immunosorbent assay （ELISA） and biochemical assays. Renal histopathological changes were observed via hematoxylin-eosin （HE） staining. IgA deposition in the renal tissue of rats was assessed by using immunofluorescence staining. The relative mRNA and protein expression levels of TLR4， NF-κB， NLRP3， and ASC in renal tissues of rats were detected by real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively.ResultsCompared with those in the blank group， the hemorrhagic spots of rats in the IgAV model group exhibited similar morphology to the rashes observed in pediatric IgAV patients. The 24-hour urinary protein quantification and urinary red blood cell counts were significantly elevated （P<0.01）. The levels of MDA， IL-18， and ICAM-1 in serum were markedly increased （P<0.01）， whereas GSH level was significantly decreased （P<0.01）. Renal histopathology reveals pronounced glomerular capillary congestion， mild degeneration and swelling of renal tubular epithelial cells， and perivascular lymphocyte infiltration. Renal immunofluorescence demonstrates a significant increase in the mean fluorescence intensity of IgA within the glomerular mesangial area （P<0.01）. Moreover， the mRNA and protein expression levels of TLR4， NF-κB p65， NLRP3， and ASC in kidney tissue were markedly upregulated （P<0.01）. Compared with those in the IgAV model group， rats in the Liangxue Tuizi prescription group and the TLR4 inhibitor group exhibited marked resolution of hemorrhagic spots. The 24-hour urinary protein quantification and urinary red blood cell counts were significantly reduced （P<0.05， P<0.01）. The levels of MDA， IL-18， and ICAM-1 in serum were markedly decreased （P<0.05， P<0.01）， whereas GSH level was significantly increased （P<0.01）. Glomerular capillary congestion was markedly alleviated. The degeneration of renal tubular epithelial cells and perivascular lymphocyte infiltration were substantially reduced. The mean fluorescence intensity of IgA within the glomerular mesangial area was significantly decreased （P<0.01）. The mRNA expression levels of TLR4， NF-κB p65， NLRP3， and ASC in renal tissue were significantly downregulated （P<0.05， P<0.01）， with the low-dose Liangxue Tuizi prescription group showing a downward trend in the mRNA expression of NF-κB p65. The protein expression levels of TLR4， phosphorylated nuclear factor‑κB p65 （p-NF-κB p65）/NF-κB p65， NLRP3， and ASC in kidney tissue were also significantly reduced （P<0.05， P<0.01）. In the low-dose Liangxue Tuizi prescription group， the protein levels of NLRP3 and ASC were markedly decreased （P<0.05）， whereas the protein levels of TLR4 and p-NF-κB p65/NF-κB p65 exhibited a downward trend.ConclusionLiangxue Tuizi prescription ameliorates urinary protein and red blood cell levels as well as reduces IgA deposition within the glomerular mesangial area. It also inhibits systemic inflammatory responses and vascular oxidative stress injury， thereby effectively attenuating vascular endothelial damage and delaying disease progression in IgAV model rats. The underlying mechanism may play a protective role against renal injury by downregulating the TLR4/NF-κB/NLRP3 signaling pathway.关键词：immunoglobulin A （IgA） vasculitis;Liangxue Tuizi prescription;Toll‑like receptor 4 （TLR4）/nuclear transcription factor-κB （NF-κB）/NOD‑like receptor protein 3 （NLRP3） signaling pathway;oxidative stress;renal injury86|36|0更新时间：2026-05-15
- 摘要：ObjectiveTo explore the mechanisms of Sargentodoxae Caulis in relieving neuropathic pain （NP） based on network pharmacology， molecular docking， and animal experiments.MethodsUltra-performance liquid chromatography-quadrupole orbitrap high-resolution mass spectrometry （UHPLC-Q-Orbitrap HRMS） was used to identify the chemical constituents of Sargentodoxae Caulis. Network pharmacology was applied to predict the core targets and related pathways of Sargentodoxae Caulis in the intervention of NP. Forty-eight Sprague-Dawley （SD） rats were randomly divided into a sham operation group， a model group， low-， medium-， and high-dose Sargentodoxae Caulis groups （1.35， 2.7， and 5.4 g·kg-1）， and a pregabalin group （30 mg·kg-1）. A NP model was established using chronic constriction injury （CCI）. The mechanical withdrawal threshold （MWT） and thermal withdrawal latency （TWL） were measured before surgery， on days 3 and 5 after surgery， and on days 3， 7， 11， and 14 after drug intervention. Immunofluorescence （IF） was used to detect the expression of neuronal excitability marker c-Fos and the neurokinin-1 receptor （NK-1R）， which is essential for central sensitization. Western blot （WB） was used to detect the protein expression and phosphorylation levels of brain-derived neurotrophic factor （BDNF）， tropomyosin receptor kinase B （TrkB）， phospholipase C-γ （PLCγ）， calcium/calmodulin-dependent protein kinase Ⅱα （CaMKⅡα）， and cAMP-response element-binding protein （CREB） in spinal cord tissue. IF was further used to detect the expression of phosphorylated TrkB （p-TrkB）， p-PLCγ， p-CaMKⅡα， and p-CREB in spinal cord tissue.ResultsA total of 138 compounds were identified in Sargentodoxae Caulis. Network pharmacology analysis revealed 409 potential targets for NP intervention， including 74 core targets such as neurotrophic tyrosine kinase receptor type 2 （NTRK2）， prostaglandin-endoperoxide synthase 2 （PTGS2）， mammalian target of rapamycin （mTOR）， serine/threonine kinase 1 （Akt1）， and mitogen-activated protein kinase 1 （MAPK1）. Molecular docking results showed that NTRK2 （encoding TrkB） exhibited good binding affinity with salidroside， sinomenine， puerarin， quercetin， naringenin， and curcumin. Behavioral results showed that， compared with the sham group， MWT and TWL were significantly decreased in the model group （P<0.01）. IF results showed that c-Fos and NK-1R expression in spinal cord tissue was significantly increased in the model group compared with the sham group （P<0.01）， while these expression levels were significantly decreased in the high-dose Sargentodoxae Caulis group compared with the model group （P<0.01）. WB and IF results showed that， compared with the sham group， the expression levels of BDNF， TrkB， p-TrkB， PLCγ， p-PLCγ， CaMKⅡα， p-CaMKⅡα， CREB， and p-CREB were significantly increased in the model group （P<0.01）. Compared with the model group， these protein expression levels were significantly decreased in the high-dose Sargentodoxae Caulis group （P<0.01）.ConclusionSargentodoxae Caulis alleviates NP by downregulating the BDNF/TrkB/CaMKⅡ/CREB signaling pathway， thereby inhibiting neuronal excitability and central sensitization.关键词：Sargentodoxae Caulis;neuropathic pain;neuronal excitability;central sensitization;brain-derived neurotrophic factor （BDNF）/tropomyosin receptor kinase B （TrkB）/calmodulin-dependent protein kinase Ⅱα （CaMKⅡα）/cAMP response element binding protein （CREB） signaling pathway104|30|0更新时间：2026-05-15
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Mechanism of Ursodeoxycholic Acid in Ameliorating Hyperlipidemia and Atherosclerosis in ApoE-/- Mice AI导读
摘要：ObjectiveAs the primary active component of traditional Chinese medicine bear bile， ursodeoxycholic acid （UDCA） has demonstrated favorable therapeutic efficacy in the clinical management of hepatobiliary diseases. To expand the clinical indications of UDCA， this study systematically investigated its ameliorative effects on hyperlipidemia and atherosclerosis， and elucidated the underlying molecular mechanisms.MethodsApolipoprotein E knockout （ApoE-/-） mice were used to establish an atherosclerosis model induced by a high-fat diet. The ApoE-/- mice were randomly divided into a control group， a high-fat model group， a positive drug ezetimibe group （5 mg·kg-1）， a low-dose UDCA group （100 mg·kg-1）， and a high-dose UDCA group （200 mg·kg-1）. Except that the control group was given a normal diet， all the other groups were fed a high-fat diet for 10 weeks， with continuous intragastric administration for 10 weeks. Body weight was measured weekly during the experiment. In the 10th week， orbital blood samples were collected following a 6 h fast. The levels of total cholesterol （TC）， triglyceride （TG）， non-high-density lipoprotein cholesterol （non-HDL-C）， and high-density lipoprotein cholesterol （HDL-C） in plasma were determined. Liver tissues were stained with hematoxylin-eosin （HE） to observe lipid deposition. Meanwhile， the aortic outflow tract tissues were harvested and stained with Oil Red O and HE to evaluate atherosclerotic plaque size. An inflammatory model was established in THP-1 mononuclear macrophages induced by lipopolysaccharide （LPS）. The cells were divided into a blank control group， an LPS model group， a low-dose UDCA group （50 μmol·L-1）， and a high‑dose UDCA group （100 μmol·L-1）. Cell viability was detected using a cell counting kit-8 （CCK-8） assay. The mRNA expression level of interleukin-6 （IL-6） in cells was measured by real-time quantitative polymerase chain reaction （Real-time PCR）. The phosphorylation levels of Janus kinase 2 （JAK2） and signal transducer and activator of transcription 3 （STAT3）， as well as the protein expression of NOD-like receptor protein 3 （NLRP3）， were determined by Western blot.ResultsIn the in vivo experiment， compared with those in the control group， the levels of plasma TC and non-HDL-C in the model group were significantly increased， while HDL-C was significantly decreased at week 10 （P<0.01）. In the model group， the liver weight and liver index of mice were enhanced （P<0.05， P<0.01）. Compared with the model group， UDCA intervention significantly reduced TC， and 200 mg·kg-1 UDCA significantly increased HDL-C （P<0.01）. UDCA also significantly decreased liver weight and liver index （P<0.05， P<0.01）， markedly reduced hepatic lipid vacuoles， alleviated steatosis， and significantly inhibited atherosclerotic plaque deposition in the aortic outflow tract. In the in vitro experiment， compared with those in the blank control group， the mRNA expression of IL-6 and the protein levels of p-STAT3 and p-JAK2/JAK2 were significantly increased in the model group （P<0.01）. Compared with the model group， 50 and 100 μmol·L-1 UDCA significantly reduced IL-6 mRNA expression （P<0.05） and p-JAK2/JAK2 （P<0.01）， and significantly decreased STAT3 phosphorylation at Tyr705 （P<0.05， P<0.01）. Under stimulation with coumermycin A1， a JAK2 agonist， both low- and high-dose UDCA significantly reduced the phosphorylation levels of JAK2 and STAT3 compared with the agonist group （P<0.01）.ConclusionUDCA ameliorates atherosclerosis through dual pathways： reducing plasma cholesterol levels and suppressing macrophage inflammation. These findings provide experimental evidence supporting the potential clinical application of UDCA in the management of hyperlipidemia and atherosclerosis.关键词：ursodeoxycholic acid;monocyte-macrophage inflammation;regulation of lipid metabolism disorders106|48|0更新时间：2026-05-15 -
Mechanisms of Qiqiao Qingwen Jiedu Granules in Alleviating Lung Injury in H1N1-infected Mice 增强出版 AI导读
摘要：ObjectiveTo investigate the protective effects and molecular mechanisms of Qiqiao Qingwen Jiedu granules （QQQW） against viral pneumonia induced by H1N1 influenza virus infection in mice.MethodsThirty-six male Balb/c mice were randomly assigned to six groups （n = 6 per group）， i.e.， blank control， model， QQQW low-dose （1.25 g·kg-1）， QQQW medium-dose （2.5 g·kg-1）， QQQW high-dose （5 g·kg-1）， and oseltamivir （20 mg·kg-1）. Except for the blank control， mice in the remaining groups were intranasally inoculated with H1N1 virus at 1.5 × LD50 to establish a pneumonia model. Drug administration began 2 hours after infection， once daily for 7 consecutive days， and relevant indicators were assessed 24 hours after the final dose. Lung pathological damage was evaluated using hematoxylin-eosin （HE） staining combined with histopathological scoring. Liquid chromatography-mass spectrometry （LC-MS） was used to identify blood-absorbed prototype components， and network pharmacology was applied to predict core targets and signaling pathways. Human non-small cell lung cancer A549 cells were used for in vitro verification， including cell counting kit-8 （CCK-8） assay， flow cytometry for apoptosis， and Western blot.ResultsCompared with the blank control， the model group showed significant increases in lung and spleen indices， lung pathological scores， and serum interleukin （IL）-17， IL-6， IL-1β， and tumor necrosis factor （TNF）-α levels （P<0.01）， along with significant decreases in phosphorylated phosphatidylinositol 3-kinase （p-PI3K）/PI3K， phosphorylated protein kinase B （p-Akt）/Akt， and phosphorylated glycogen synthase kinase 3β （p-GSK3β）/GSK3β ratios in lung tissue （P<0.01）. All QQQW dose groups significantly reduced organ indices， pathological scores， and pro-inflammatory cytokine levels （P<0.05）， with the high-dose group showing effects comparable to oseltamivir. The high-dose QQQW group significantly upregulated phosphorylated protein ratios in the PI3K/Akt/GSK3β pathway （P<0.01）. In A549 cells， 100 mg·L-1 QQQW significantly increased cell viability， decreased apoptosis， and upregulated phosphorylated protein ratios in this pathway compared with the H1N1 infection model group （P<0.01）. These effects were reversed by the PI3K inhibitor LY294002 （P<0.01）. Network pharmacology analysis identified GSK3β as a key target and PI3K/Akt as the core pathway of QQQW.ConclusionQQQW （1.25-5 g·kg-1） dose-dependently alleviates H1N1-induced lung inflammation and tissue damage by activating the PI3K/Akt/GSK3β signaling pathway. The high dose （5 g·kg-1） shows comparable efficacy to oseltamivir （20 mg·kg-1）.关键词：Qiqiao Qingwen Jiedu Granules;H1N1 influenza virus;phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/glycogen synthase kinase 3β （GSK3β） signaling pathway;lung injury;network pharmacology86|77|0更新时间：2026-05-15 - 摘要：ObjectiveThis study aims to investigate the effects of Qijiang Yimai prescription on vascular aging of type 2 diabetes mellitus （T2DM） rats， the fibroblast growth factor 21/adenosine monophosphate-activated protein kinase （FGF21/AMPK） signaling pathway， and mitophagy.MethodsEight rats were selected randomly from a total of 48 SPF-grade male SD rats as the blank group， while the remaining 40 rats were fed a high-sugar and high-fat diet combined with a low dose of streptozotocin （STZ） to establish a T2DM rat model. The rats were then divided into a model group， Qijiang Yimai prescription groups with low， medium， and high doses （3.72， 7.44， and 14.88 g·kg-1）， and a metformin group （132.9 mg·kg-1）， with eight rats per group. Rats in the treatment groups received corresponding doses of Qijiang Yimai prescription and metformin by gavage， while those in the blank and model groups were given an equivalent volume of double-distilled water for eight weeks consecutively. Hematoxylin-eosin （HE） staining was performed to observe histopathological changes in vascular tissues. Levels of endothelial microparticles （EMPs） in serum and senescence-associated secretory phenotype （SASP） in vascular tissues were measured by enzyme-linked immunosorbent assay （ELISA）. The expressions of tumor protein p53 （p53） and cyclin-dependent kinase inhibitor 1A （p21） in vascular tissues were examined by using immunohistochemistry （IHC）. Western blot and real-time quantitative polymerase chain reaction （Real-time PCR） were employed to detect protein and mRNA expression levels of FGF21， fibroblast growth factor receptor 1 （FGFR1）， β-Klotho （KLB）， liver kinase B1 （LKB1）， phosphorylated AMP-activated protein kinase （p-AMPK）， AMPK， PTEN-induced serine/threonine kinase 1 （PINK1）， E3 ubiquitin ligase （Parkin）， and sequestosome-1 （p62）.ResultsCompared with those in the blank group， rats in the model group showed marked aging-related pathological alterations in the histomorphology of the carotid artery tissues， accompanied by significantly increased EMP levels in serum （P<0.01）. The levels of interleukin-1β （IL-1β）， IL-8， matrix metalloproteinase‑1 （MMP-1）， and MMP-9 in vascular tissues were also significantly elevated （P<0.01）. Protein expression levels of p53 and p21 were notably increased （P<0.05， P<0.01）. In contrast， the protein and mRNA expression levels of FGF21， FGFR1， KLB， LKB1， the p-AMPK/AMPK ratio， PINK1， and parkin were significantly reduced （P<0.01）， while the protein and mRNA expression levels of p62 were markedly upregulated （P<0.01）. Compared with those in the model group， the rats in all treatment groups exhibited varying degrees of improvement in aging-related pathological alterations of the carotid artery tissues. The levels of EMPs in serum and SASP in vascular tissues were reduced to different extents （P<0.01）. Expression levels of p53 and p21 were also decreased to varying degrees （P<0.05， P<0.01）. Meanwhile， the protein and mRNA expression levels of FGF21， FGFR1， KLB， LKB1， p-AMPK， AMPK， PINK1， and parkin were elevated to varying degrees （P<0.05， P<0.01）， whereas the protein and mRNA expression levels of p62 were reduced to varying degrees （P<0.05， P<0.01）.ConclusionQijiang Yimai prescription can intervene aging and inflammatory injury in vascular tissues of T2DM rats， and its mechanism may be associated with upregulation of the FGF21/AMPK signaling pathway and enhancement of mitophagy.关键词：Qijiang Yimai prescription;type 2 diabetes mellitus;vascular aging;fibroblast growth factor 21;mitophagy87|32|0更新时间：2026-05-15
- 摘要：ObjectiveTo study the mechanism of inflammatory injury and microangiogenesis disorder in diabetic mice with ovarian dysfunction and the intervention effect of modified Sanjiasan.MethodsDiabetic model mice were established by high-glucose and high-fat diet combined with streptozotocin （STZ）， and the model of diabetic mice with ovarian dysfunction was established after confirming estrous cycle disorder through vaginal smear examination. Forty successfully modeled mice were randomly assigned to five groups： a model group， high- （17.94 g·kg-1）， medium- （8.97 g·kg-1）， and low-dose （4.49 g·kg-1） modified Sanjiasan groups， and a western medicine group （metformin， 0.2 g·kg-1）. Eight mice from the same batch were selected as the blank control group. After 28 days of consecutive intragastric administration， fasting blood glucose （FBG） was measured. The serum levels of inhibin B （INHB）， estradiol （E2）， follicle-stimulating hormone （FSH）， anti-Müllerian hormone （AMH）， luteinizing hormone （LH）， tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and monocyte chemoattractant protein-1 （MCP-1） were assessed by enzyme-linked immunosorbent assay （ELISA）. Ovarian histopathology and follicle count were evaluated via hematoxylin-eosin （HE） and Masson staining. Ultrastructure was observed by transmission electron microscopy （TEM）. Apoptosis of ovarian granulosa cells was detected via terminal deoxynucleotidyl transferase dUTP nick end labeling （TUNEL） assay. Microvascular density in ovary was quantified by immunofluorescence. The expression of vascular endothelial growth factor （VEGF）， platelet-derived growth factor （PDGF）， Claudin-5， zonula occludens-1 （ZO-1）， 70-kDa ribosomal protein S6 kinase 1 （p70S6K1）， myeloid differentiation primary response protein 88 （MyD88）， and nuclear factor kappa B （NF-κB） was analyzed using immunohistochemistry and Western blot.ResultsCompared with the blank control group， the model group exhibited significantly elevated FBG， FSH， LH， TNF-α， IL-6， and MCP-1 levels （P<0.01）， decreased E2， AMH， and INHB levels （P<0.01）， poor follicular development， an increased collagen fiber area （P<0.01）， impaired ultrastructure of ovarian tissue， a decreased number of microvessels （P<0.01）， an increased TUNEL-positive rate （P<0.01）， reduced protein expression levels of VEGF， PDGF， Claudin-5， ZO-1， and p70S6K1 （P<0.01）， and increased MyD88 and NF-κB expression （P<0.01）. Compared with the model group， the high- and medium-dose modified Sanjiasan groups and the western medicine group showed decreased levels of FBG， FSH， LH， TNF-α， IL-6， and MCP-1 （P<0.01）， increased levels of E2， AMH， and INHB （P<0.01）， improved ovarian follicular development， a reduced collagen fiber area （P<0.01）， improved ultrastructure of ovarian tissue， an increased number of microvessels （P<0.01）， a decreased TUNEL-positive rate （P<0.01）， upregulated protein expression levels of VEGF， PDGF， Claudin-5， ZO-1， and p70S6K1 （P<0.01）， and downregulated protein expression levels of MyD88 and NF-κB （P<0.01）. None of these improvements were statistically significant in the low-dose modified Sanjiasan group.ConclusionModified Sanjiasan improves ovarian reserve in diabetic mice with ovarian dysfunction by reducing blood glucose， regulating hormones， promoting microangiogenesis， and modulating the MyD88/NF-κB signaling pathway.关键词：modified Sanjiasan;type 2 diabetes mellitus;ovarian dysfunction;microangiogenesis;inflammation96|47|0更新时间：2026-05-15
- 摘要：ObjectiveTo investigate the inhibitory effects of quercetin on hepatocellular carcinoma（HCC） cells and the potential mechanisms by which it exerts its activity through the glycolytic pathway.MethodsHuh-7 and MHCC-97H HCC cells were treated with different concentrations of quercetin（0-500 μmol·L-1）. Cell viability was assessed using the cell counting kit-8（CCK-8） assay， and the half-maximal inhibitory concentration（IC50） values were calculated to determine the appropriate intervention concentrations. Cells were divided into a control group， a dimethyl sulfoxide（DMSO） group， and quercetin low-， medium-， and high-concentration groups. Colony formation assay， wound healing assay， and Transwell assay were performed to evaluate cell proliferation， migration， and invasion， respectively. Differentially expressed genes（DEGs） were identified using RNA sequencing（RNA-seq）， followed by Gene Ontology（GO） functional enrichment and Kyoto Encyclopedia of Genes and Genomes（KEGG） pathway analysis. A protein-protein interaction（PPI） network was constructed， and potential hub targets were screened using the edge percolated component（EPC） algorithm. Glucose uptake was detected using a fluorescent probe assay， lactate production was measured by a colorimetric method， and the mRNA and protein expression levels of candidate targets were examined using real-time quantitative polymerase chain reaction（Real-time PCR） and Western blot， respectively.ResultsQuercetin inhibited the proliferation of HCC cells in a concentration- and time-dependent manner（P<0.01）. The IC50 values of quercetin in Huh-7 cells at 24， 48， 72 h were 231.0， 94.3， 75.4 μmol·L-1， respectively， while those in MHCC-97H cells were 588.8， 184.1， 132.0 μmol·L-1. It also significantly reduced colony formation， decreased the number of migrating and invading cells in Transwell assays， and lowered wound healing rates（P<0.01）. In addition， glucose uptake and lactate production were markedly suppressed（P<0.01）. RNA-seq identified a total of 821 DEGs， including 399 upregulated and 422 downregulated genes［|log2fold change（FC）| ≥1， adjusted P<0.05］. Hierarchical clustering analysis revealed distinct gene expression patterns between groups. GO enrichment analysis showed that DEGs were mainly enriched in biological processes such as hypoxia response， oxygen level regulation， and pyruvate metabolism， cellular components including collagen-containing extracellular matrix and external side of the plasma membrane， and molecular functions such as carboxylic acid binding and lyase activity（P<0.05）. KEGG analysis indicated significant enrichment in glycolysis/gluconeogenesis， carbon metabolism， and the hypoxia inducible factor-1（HIF-1） signaling pathway（P<0.05）. PPI combined with EPC algorithm identified six key glycolysis-related genes， including solute carrier family 2 member 1（SLC2A1）， pyruvate kinase M（PKM）， phosphoglycerate kinase 1（PGK1）， enolase 2（ENO2）， fructose-bisphosphate aldolase A（ALDOA）， and glucose-6-phosphate isomerase（GPI）. Real-time PCR and Western blot results further confirmed that quercetin dose-dependently downregulated the mRNA and protein expression levels of these six core genes（P<0.01）.ConclusionQuercetin suppresses glycolytic activity and inhibits the proliferation， migration， and invasion of HCC cells by downregulating key glycolysis-related genes， including SLC2A1， PKM， and PGK1， thereby impeding the malignant progression of HCC. These findings suggest that quercetin has potential as a natural candidate compound for anti-HCC therapy.关键词：quercetin;hepatocellular carcinoma;glycolysis;hypoxic response;solute carrier family 2 member 1（SLC2A1）;pyruvate kinase M（PKM）;phosphoglycerate kinase 1（PGK1）84|44|0更新时间：2026-05-15
- 摘要：Neutrophil extracellular traps （NETs）， as a key effector mechanism of the immune system， are reticular structures composed of disaggregated chromatin skeletons and neutrophil granule proteins. Substantial evidence indicates that NETs exert dual regulatory roles in the initiation and progression of chronic heart failure （CHF）. On the one hand， NETs exacerbate myocardial fibrosis and ventricular remodeling by releasing proinflammatory factors through the release of damage-associated molecular patterns （DAMPs） and granzyme enzymes. On the other hand， NETs indirectly participate in myocardial microenvironment repair by regulating collagen degradation balance through trapping matrix metalloproteinases and promoting the expression of vascular endothelial growth factors. Precision regulation of NETs， which exert dual effects in promoting inflammatory damage and mediating tissue repair in CHF， represents a core section and critical step for treating chronic heart failure. Traditional Chinese medicine demonstrates unique advantages in regulating the dual effects of NETs， offering multi-level， multi-pathway intervention strategies for CHF treatment. However， the specific regulatory mechanisms remain unclear. This paper focused on the role of NETs in the pathophysiological process of CHF， delving into their specific action pathways within the inflammatory response. It explored the impact of NETs on myocardial tissue repair， identifying potential therapeutic targets and modes of action. By comprehensively reviewing and analyzing current Chinese and international research findings， this study aims to provide innovative research approaches and methodologies for NETs-related research in the clinical management of CHF.关键词：neutrophil extracellular trap;chronic heart failure;traditional Chinese medicine;inflammatory response;tissue repair110|73|0更新时间：2026-05-15
- 摘要：Chronic heart failure（CHF）， representing the terminal stage of the cardiovascular system， involves complex pathological mechanisms. These encompass structural and functional alterations in cardiomyocytes， alongside multiple pathological processes such as heightened systemic inflammation， elevated oxidative stress levels， and vascular dysfunction. Neutrophil extracellular traps（NETs） are reticular structural complexes released by neutrophils in response to specific stimuli， serving a bactericidal defense function. Recent studies reveal that NET dysregulation can induce myocardial tissue damage， trigger inflammatory immune responses， and promote a hypercoagulable blood state， playing a significant role in the initiation and progression of CHF. Therefore， modulating NET status holds promise as a novel therapeutic target for CHF. Traditional Chinese medicine theory posits that "deficiency， stasis， and toxin" constitute the core pathogenesis in the initiation and development of CHF. Among these， "deficiency" represents the fundamental cause， predominantly observed in the early stage and persisting throughout the disease course. "Stasis" manifests as a localized pathological presentation， serving as the primary pathogenesis during the middle stage of CHF. "Toxin" signifies the manifestation and emerges as the principal pathogenic factor in the late stage of CHF. The pathological effects of NET imbalance align closely with the "deficiency， stasis， and toxin" pathogenesis theory in traditional Chinese medicine. The NET imbalance phenomenon observed in CHF was integrated with the "deficiency， stasis， and toxin" pathogenesis theory in traditional Chinese medicine. Declining cardiac function corresponds to "deficiency". Inflammatory immune responses correspond to "toxin". Hypercoagulable blood state corresponds to "stasis". The intrinsic connection between NETs and CHF pathogenesis was elucidated from this perspective. In line with traditional Chinese medicine characteristics， this paper emphasized treatment based on syndrome identification and etiology identification through syndrome analysis. Clinical therapeutic methods were summarized with representative formulas： Tonifying deficiency（Nuanxin Kang）， resolving stasis（Qingxin Jieyu Granules）， and eliminating toxins（optimized formula for phlegm-stasis concurrent treatment）. This will provide a novel perspective for the integrated Chinese and Western medicine treatment of CHF.关键词：chronic heart failure;deficiency， stasis， and toxin;neutrophil extracellular trap;traditional Chinese medicine;traditional Chinese medicine theory94|41|0更新时间：2026-05-15
- 摘要：Chronic heart failure （CHF） is a clinical syndrome in which primary myocardial injury leads to structural and/or functional alterations of the heart， resulting in impaired cardiac pumping and/or filling function. It is characterized by high incidence， high hospitalization rates， and high mortality， and remains a major focus and challenge in current research. In traditional Chinese medicine （TCM）， it is classified into categories such as "heart impediment"， "cardiac edema"， and "heart distension"， and represents the terminal stage of various heart-related diseases. The theory of "Zhu-Ke interaction" was proposed by the warm disease scholar WU Youxing， in which "Zhu" refers to the healthy Qi and "Ke" to pathogenic Qi. Deficiency of healthy Qi allows pathogenic Qi to invade， leading to entanglement between the two， prolonged disease course， and eventual formation of chronic refractory conditions. Based on this theory， this article systematically analyzes and discusses the pathogenesis characteristics， therapeutic principles， and prescription strategies for CHF， with the aim of providing new ideas and methods for its diagnosis and treatment. The authors propose that the core pathogenesis of CHF consists of deficiency of Zhu Qi， invasion of Ke Qi， and simultaneous involvement of both. The fundamental therapeutic principle is to reinforce the healthy Qi， eliminate pathogenic factors， and separate Zhu from Ke. The basic treatment methods include tonifying Qi， warming Yang， unblocking the meridians， and promoting diuresis. At the same time， syndrome differentiation and treatment should be conducted in stages according to disease progression and syndrome characteristics. In the early stage， when Zhu and Ke have just interacted and the deficiency of Zhu is relatively mild， common syndrome patterns include Qi deficiency with blood stasis， and treatment should focus on tonifying Qi and activating blood circulation. In the middle stage， when Zhu and Ke are intertwined and both deficiency and excess are equally prominent， common patterns include Yang deficiency with blood stasis and Yang deficiency with fluid retention， and treatment should focus on warming Yang， promoting blood circulation， and inducing diuresis. In the late stage， when Zhu declines and Ke prevails and their interaction becomes difficult to resolve， common patterns include deficiency of both Qi and Yin and sudden collapse of heart Yang， and treatment should therefore aim to restore Yang and rescue collapse， and to separate and eliminate Zhu and Ke. In addition， this theory may also be extended to the treatment of other diseases.关键词：chronic heart failure;"Zhu-Ke-interaction" theory;reinforce the healthy Qi， eliminate pathogenic factors;separate Zhu from Ke;syndrome differentiation and treatment92|48|0更新时间：2026-05-15
- 摘要：ObjectiveThis paper aims to explore the mechanism of action of Danhong injection inducing oxidative stress in chronic heart failure based on silent information regulator 1 （SIRT1）/nuclear factor-erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） pathway.MethodsSPF male SD rats were randomly divided into a sham operation group， a model group， a captopril group （8.8 mg·kg-1）， and a Danhong injection group （6.0 mL·kg-1）. The model group was prepared by abdominal aortic coarctation， and the sham operation group was only operated by laparotomy without ligation. After 15 days of administration， echocardiography was used to detect the cardiac color Doppler ultrasound. Enzyme-linked immunosorbent assay （ELISA） was used to determine the content of N-terminal pro-brain natriuretic peptide （NT-proBNP） in the serum of each group， and the contents of superoxide dismutase （SOD）， glutathione peroxidase （GPX）， catalase （CAT）， malondialdehyde （MDA）， and total antioxidant capacity （T-AOC） were detected. The pathological changes of myocardial tissue were detected by hematoxylin-eosin （HE） and Masson staining， and the fibrosis rate was calculated. Terminal-deoxynucleotidyl transferase-mediated dUTP nick end labeling assay （TUNEL） method was used to count apoptotic positive nuclei. The expression levels of SIRT1， Nrf2， HO-1， GPX， CAT， SOD， B lymphocyte tumor-2 （Bcl-2）， B-cell lymphoma-2 associated protein X （Bax）， and cysteine protease 3（Caspase-3） were detected by Western blot. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to analyze the mRNA expression levels of SIRT1， Nrf2， and HO-1.ResultsCompared with those in the sham operation group， HE and Masson staining of the myocardium showed compensatory hypertrophy and fibrosis of the myocardium， and a large number of inflammatory cells were infiltrated. Left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） were significantly decreased （P<0.01）， while left ventricular internal end-diastolic diameter （LVIDd） and left ventricular internal end-systolic diameter （LVIDs） were significantly increased （P<0.01）. The contents of NT-proBNP， MDA， and T-AOC in serum were increased significantly （P<0.01）， while the activities of SOD， CAT， and GPX were decreased significantly （P<0.01）. The apoptosis rate was significantly increased （P<0.01）. The protein expressions of Bax and Caspase-3 in myocardium were significantly increased （P<0.01）， while the protein and mRNA expressions of GPX， CAT， SOD， Bcl-2， SIRT1， Nrf2， and HO-1 were significantly decreased （P<0.01）. Compared with those in the model group， LVIDd and LVIDs in the Danhong injection group were significantly decreased （P<0.05， P<0.01）， and LVEF and LVFS were significantly increased （P<0.05， P<0.01）. The contents of NT-proBNP， MDA， and T-AOC in serum were significantly decreased （P<0.05， P<0.01）. The activities of SOD， CAT， and GPX were increased （P<0.01）. HE and Masson staining of the myocardium show that compensatory hypertrophy of the myocardium was relieved， and the fibrosis was reduced. The number of TUNEL positive cells was decreased （P<0.01）. The protein and mRNA expressions of GPX， CAT， SOD， Bcl-2， SIRT1， Nrf2， and HO-1 in myocardium were increased significantly （P<0.05， P<0.01）， while the protein expressions of Bax and Caspase-3 were decreased significantly（P<0.01）.ConclusionDanhong injection can achieve its regulatory effect by activating the SIRT1/Nrf2/HO-1 signaling pathway， inhibit the level of oxidative stress， and play a role in protecting myocardial tissue and improving cardiac function.关键词：chronic heart failure;oxidative stress;silent information regulator 1 （SIRT1）/nuclear factor-erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway;Danhong injection41|38|0更新时间：2026-05-15
- 摘要：Chronic heart failure （CHF） is the terminal stage of various heart diseases， characterized by high prevalence， high mortality， and high symptom burden. The Yin-Yang theory， an essential foundation of traditional Chinese medicine （TCM） theories， is used to explain human physiology and pathology as well as guide diagnosis and treatment. Qi and Yin deficiency is the core pathogenesis of CHF. Insufficient Yangqi results in weak circulatory propulsion， while Yin deficiency leads to inadequate nourishment of the heart vessels， causing an imbalance of Yin and Yang in the body. Shengmai San， a classical formula for tonifying Qi and nourishing Yin， consists of Ginseng， Ophiopogon， and Schisandra， containing various active compounds such as ginsenosides， steroidal saponins， high-isoflavones， lignans， terpenoids， and flavonoids， which have notable effects on cardiovascular diseases. The therapeutic effects of Shengmai San-type formulas on CHF are mainly associated with mechanisms such as improving cardiac function， inhibiting inflammatory responses， reducing cardiomyocyte apoptosis， preventing ventricular remodeling and myocardial fibrosis， countering oxidative stress， and regulating the neuroendocrine system. The treatment method centers on tonifying Qi and nourishing Yin， addressing the fundamental Qi and Yin deficiency while also considering concomitant syndromes such as blood stasis and stagnation， internal heat due to Yin deficiency， Qi and Yang deficiency， and water retention. The therapy is based on replenishing Qi， generating fluids， consolidating Yin， and restoring the pulse， and it is supplemented according to the syndrome with methods for promoting blood circulation， clearing heat， warming Yang， and promoting urination， thereby harmonizing Yin and Yang in accordance with the "deficiency in root， excess in branch" pathogenesis of CHF. This study， grounded in Yin-Yang theory， investigated the etiology and pathogenesis of CHF， as well as the formulation characteristics， material basis， and mechanisms of action of Shengmai San-type formulas in the treatment of CHF， aiming to provide a theoretical foundation and reference for the clinical practice and scientific research of Shengmai San-type formulas.关键词：Yin-Yang theory;Shengmai San;chronic heart failure（CHF）;mechanism of action;myocardial fibrosis103|72|0更新时间：2026-05-15
- 摘要：ObjectiveTo observe the safety and efficacy of Sangxing Zhike granules in the treatment of post-infectious cough （PIC） with the syndrome of pathogenic dryness invading the lung， and to preliminarily explore their regulatory effect on inflammatory factors.MethodsA randomized， double-blind， placebo-controlled parallel trial was designed. A total of 110 patients diagnosed with PIC and identified as having the syndrome of pathogenic dryness invading the lung were recruited from the patients who visited the department of respiratory and critical care medicine at Xinjiang Uygur autonomous region hospital of traditional Chinese medicine from November 2024 to October 2025. Patients were randomly assigned to the control group （placebo+compound Methoxyphenamine capsules） and the observation group （Sangxing Zhike granules+compound Methoxyphenamine capsules）， with 55 cases in each group. Basic information， medical history， traditional Chinese medicine （TCM） syndrome scores， cough evaluation test （CET） scores， cough symptom scores， visual analogue scale （VAS） scores， Leicester cough questionnaire （LCQ） scores， and laboratory test results of the patients were collected before treatment and after 14 days of treatment. Exhaled breath condensate （EBC） was collected from the patients before treatment and after 14 days of treatment， and changes in airway inflammatory cytokines were detected using enzyme-linked immunosorbent assay （ELISA） kits. TCM syndrome scores， CET scores， cough symptom scores， VAS scores， and LCQ scores of the patients were collected via telephone 30 days after medication.ResultsA total of 94 cases completed the trial， including 45 cases in the control group and 49 cases in the observation group. The total effective rate of the observation group was 93.9%（46/49）， significantly higher than the 77.8%（35/45） of the control group （χ2=5.102，P<0.05）. The scores of cough frequency， cough severity， expectoration， dry throat， dryness of the lips and nose， itchy throat， dry mouth and thirst in the observation group were significantly decreased after 2 weeks of treatment and 1 month after treatment （P<0.05）. Compared with the patients' scores before treatment， the CET scores， cough symptom scores， VAS scores， and TCM syndrome scores of both groups decreased significantly at 2 weeks of treatment and 1 month after treatment， while the LCQ scores increased significantly （P<0.05）. In comparison with the control group at 2 weeks of treatment and 1 month after treatment， the CET scores， cough symptom scores， VAS scores， and TCM syndrome scores of the observation group decreased significantly at 2 weeks and 1 month after treatment， while the LCQ scores increased significantly （P<0.05）. Based on the LCQ score for quality of life comparison， the physiological， psychological， and social scores of the observation group and the control group at 2 weeks and 1 month after treatment were significantly higher than those before treatment （P<0.05）. Compared with the control group at 2 weeks and 1 month after treatment， the observation group exhibited significantly increased physiological， psychological， and social scores at 2 weeks and 1 month after treatment （P<0.05）. The recurrence rate of the observation group （18.4%，9/49） was significantly lower than that of the control group（51.1%，23/45） （χ2=2.174，P<0.05）. The median recovery time of the observation group was 7（5，10） days， significantly shorter than 11（8，12） days of the control group （P<0.05）. Compared with the scores before treatment in the same group， the levels of TNF-α， IFN-γ， IL-4， IL-5， and IL-13 in EBC after 2 weeks and 1 month of treatment were significantly lower in both groups （P<0.05）. Compared with the control group after 2 weeks of treatment， IL-13 in the observation group after 2 weeks of treatment was significantly increased （P<0.05）. In addition， Sangxing Zhike granules showed favorable safety performance， with no differences in complete blood count， hepatic and renal function within and between groups.ConclusionThe combination of Sangxing Zhike granules and compound Methoxyphenamine capsules is effective in treating PIC with syndrome of pathogenic dryness invading the lung， significantly improving the cure rate， shortening the median recovery time， reducing the recurrence rate， and significantly improving TCM syndrome scores， CET scores， cough symptom scores， VAS scores， and LCQ scores， with favorable safety.关键词：Sangxing Zhike granules;post-infectious cough;pathogenic dryness invading the lung;randomized， double-blind， placebo-controlled parallel-group trial;Sangxing Tang81|38|0更新时间：2026-05-15
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Clinical Evidence Map Analysis of Traditional Chinese Medicine Treatment of Menopausal Syndrome 增强出版 AI导读
摘要：ObjectiveMenopausal syndrome （MPS） is a common health issue that occurs before and after menopause due to fluctuations in sex hormones. Traditional Chinese medicine （TCM）， with its multi-target regulation and minimal side effects， has gradually become an important alternative to menopausal hormone therapy （MHT）. Therefore， this study systematically integrates and evaluates the clinical evidence of TCM treatment of MPS through an evidence map.MethodsThis study used an evidence map to systematically review 917 articles （including 870 interventional studies， 18 observational studies， 24 Meta-analyses， and 5 guidelines） from Chinese and English databases that were published between 2015 and 2024， comprehensively analyzing the distribution characteristics of clinical evidence for TCM treatment of MPS.Results① The research intensity of TCM treatment of MPS reached its peak in 2021 and declined slightly in the past two years. The sample size of studies was concentrated between 60 and 100 cases， with an observation period primarily of 3 months. ② Hot intervention measures were concentrated on integrated traditional and Western medicine therapy （51.9%）， with high-frequency intervention measures being Kuntai capsules （53.6%） and Erxian Tang （12.1%）. The core syndromes primarily involved liver-kidney Yin deficiency （24.6%） and liver depression and kidney deficiency （18.2%）. ③ Outcome indicators prioritized clinical efficacy and hormone levels， while insufficient attention was paid to TCM symptom scores， mental health， sleep disorders， and long-term symptoms （such as cognitive function and osteoporosis）. ④ Methodological quality urgently needs improvement， as randomized controlled trials （RCTs） had issues in random sequence generation， allocation concealment， and blinding implementation， which resulted in a high risk of bias. Meta-analyses/systematic reviews primarily faced challenges in study protocol registration， exclusion criteria， publication bias， and heterogeneity interpretation.ConclusionTCM treatment of MPS has therapeutic advantages， while there are issues with research design standardization and fragmented evidence. Future efforts should focus on promoting large-scale， multi-center studies. Secondly， in interventional studies， the evaluation dimensions of outcome indicators are relatively limited. In the future， drug efficacy should be evaluated from multiple dimensions based on the “bio-psycho-social” evaluation framework. Additionally， a core outcome set （COS） for TCM treatment of MPS should be established and optimized to improve research quality and provide strong support for TCM treatment of MPS.关键词：traditional Chinese medicine;menopausal syndrome;evidence map;randomized controlled trial;systematic review107|45|0更新时间：2026-05-15 - 摘要：ObjectiveTo initially explore the clinical efficacy of the internal administration of the Tongluo Zhibi formula combined with external treatment of meridian sinew manipulation on patients with knee osteoarthritis （KOA）， and to observe its influence on serum biomarkers of cartilage metabolism and biomechanical function of the knee joint.MethodsFrom April 2025 to November 2025， 80 patients with unilateral KOA were randomly divided into a control group （40 cases） and a treatment group （40 cases）. Among them， 10 cases dropped out in the control group and 5 cases in the treatment group. In the control group， there were 10 males and 20 females； 17 cases involved the left knee and 13 cases the right knee； age ranged from 43 to 73 years， with an average of （61.76±7.92） years； disease duration ranged from 9 to 35 weeks， with an average of （18.27±7.85） weeks； K-L X-ray grades were grade Ⅰ in 20 cases， grade Ⅱ in 6 cases， and grade Ⅲ in 4 cases. The control group was treated with oral celecoxib and glucosamine combined with physical therapy. In the treatment group， there were 12 males and 23 females； 16 cases involved the left knee and 19 cases the right knee； age ranged from 41 to 75 years， with an average of （59.89±9.04） years； disease duration ranged from 12 to 42 weeks， with an average of （21.63±7.38） weeks； K-L X-ray grades were grade Ⅰ in 12 cases， grade Ⅱ in 10 cases， and grade Ⅲ in 5 cases. The treatment group was treated with Tongluo Zhibi Formula combined with meridian sinew manipulation. The Western Ontario and McMaster Universities Osteoarthritis Index （WOMAC） scores， serum cartilage metabolism markers （CTX-Ⅱ， COMP）， gait parameters （step length， gait speed， double support phase）， muscle tone of the quadriceps and gastrocnemius on the affected side， and quality of life survey （SF-36 score） were compared between the two groups before and after treatment. Safety and adverse events were also evaluated.ResultsBoth the treatment group and the control group showed significant improvements in WOMAC scores for pain， stiffness， joint function， and total score compared with those before treatment （P<0.05）， and the improvement in the treatment group was more significant （P<0.05）. After treatment， both groups showed significant improvements in CTX-Ⅱ， COMP， step length， gait speed， and double support phase （P<0.05）， and the improvement in the treatment group was better than that in the control group （P<0.05）. Before treatment， there were no statistically significant differences in the displacement values of muscle tone of the quadriceps and gastrocnemius on the affected side and SF-36 scores between the two groups. After treatment， the displacement values of muscle tension of the quadriceps and gastrocnemius on the affected side and SF-36 scores in both groups were significantly improved compared with those before treatment （P<0.05）， and the improvement in the treatment group was more significant than that in the control group （P<0.05）. No serious adverse events occurred in either group， indicating good safety.ConclusionThe Tongluo Zhibi formula combined with meridian sinew manipulation in the treatment of KOA with liver-kidney deficiency and phlegm-stasis intermingling syndrome shows potential superiority over simple Western medicine treatment in short-term clinical efficacy， improvement of cartilage metabolism indicators， and enhancement of biomechanical function， with good safety. These findings provide preliminary modern medical evidence for the theory of "simultaneous treatment of both tendons and bones".关键词：knee osteoarthritis;Tongluo Zhibi formula;meridian sinew manipulation;biomechanics;cartilage metabolism;randomized controlled trial74|28|0更新时间：2026-05-15
- 摘要：ObjectiveThis paper aims to construct volatile organic compound fingerprint profiles of different origins in Magnoliae Flos medicinal materials produced in Henan province and elucidate the differences in volatile organic compound components of different origins in Magnoliae Flos medicinal materials produced in Henan province， so as to achieve precise identification of different origins in Magnoliae Flos medicinal materials produced in Henan province.MethodsThe combination of gas chromatography-mass spectrometry （GC-MS） and gas chromatography-ion mobility spectrometry （GC-IMS） technology was used to detect the volatile organic compounds of three varieties of Magnoliae Flos medicinal materials produced in Henan province： Yulan， Damaotao， and Xiaomaotao. The differences in volatile organic compounds of the three varieties were compared and analyzed. The Gallery Plot plug-in of LAV software was used to conduct fingerprint profile analysis， and the difference peaks screened out by the fingerprints were analyzed with the help of the principal component analysis （PCA） method， thereby studying and identifying the origins of Magnoliae Flos medicinal materials as well as establishing the criteria for the identification of the origins.ResultsGC-MS was used to screen 16 volatile components in Damaotao， 14 volatile components in Xiaomaotao， 9 volatile components in Yulan， and 7 common volatile components. Based on the built-in NIST database and IMS database of the software， a total of 51 volatile organic compounds were identified from the three kinds of Magnoliae Flos medicinal materials， including alcohols （16 kinds）， alkenes （13 kinds）， aldehydes （10 kinds）， esters （5 kinds）， ketones （5 kinds）， pyrazines （1 kind）， and benzenes （1 kind）. The peak intensities of some volatile organic compounds in the three kinds of Magnoliae Flos were significantly different， and the fingerprint profile and peak height were further compared， revealing that 43 volatile organic compounds with significant content differences existed among the three kinds of Magnoliae Flos， including 14 kinds of high-content components in Yulan， 10 kinds in Damaotao， and 19 kinds in Xiaomaotao. Among the compounds in Yulan， the relative content of alkenes was higher， while the relative contents of alcohols， aldehydes， ketones， and benzene compounds were higher in Damaotao， and the relative content of esters was higher in Xiaomaotao.ConclusionThe organic volatile components of Magnoliae Flos medicinal materials can be compared and analyzed by the combination of GC-MS and GC-IMS technology， and the Magnoliae Flos medicinal materials with different origins can be quickly and accurately identified， which provides an important reference for the research on the overall differences of Magnoliae Flos medicinal materials with different origins in the later stage and provides a scientific basis for the quality control and application of such medicinal materials.关键词：Magnoliae Flos;volatile component;gas chromatography-ion mobility spectrometry （GC-IMS）;gas chromatography-mass spectrometry （GC-MS）96|74|0更新时间：2026-05-15
- 摘要：ObjectiveTo rapidly identify the chemical constituents of Yinchen Wulingsan and its absorbed components in the serum and tissues of mice by ultra-high performance liquid chromatography-quadrupole-orbitrap high resolution mass spectrometry（UHPLC-Q-Orbitrap HRMS）.MethodsHealthy male C57/BL6J mice（n=12） were divided into the blank group（n=3） and treatment group（n=9）. The blank group received purified water via intragastric administration， while the treatment group was given Yinchen Wulingsan extract at a dose of 10.28 g·kg-1 via intragastric administration. At 0.5， 1.5， 3 h post-administration， 3 mice from the treatment group were processed at each time point. Serum and tissue samples from the lung， heart， spleen， liver， kidney， and ileum were collected. Following MS data acquisition， the relative retention time of ion peaks and accurate relative molecular mass were integrated， and elemental compositions were fitted using Xcalibur 4.2 software. The chemical constituents of Yinchen Wulingsan， as well as the prototype compounds absorbed into the blood and distributed in various tissues， were identified by comparing secondary MS fragmentation information with reference substances， literature， and database entries.ResultsA total of 208 chemical constituents were identified from Yinchen Wulingsan， including 107 terpenoids， 41 flavonoids， 23 organic acids， 11 compounds of other categories， 10 steroids， 10 coumarins， and 3 compounds each of alkaloids and anthraquinones. At 0.5， 1.5， 3 h after intragastric administration of Yinchen Wulingsan to mice， 48， 43， 40 prototype components were detected in the serum， respectively. Additionally， 56， 32， 45， 56， 50， 59 prototype components were identified in the lung， heart， liver， spleen， kidney， and ileum， respectively. Among these， twenty components such as alisol A， capillartemisin A and alisol J-23-acetate were detected in both the serum and all examined tissues， suggesting they may serve as the potential active constituents.ConclusionThis study identifies terpenoids， flavonoids， and organic acids as the main constituents of Yinchen Wulingsan， providing a reference for subsequent pharmacokinetic studies of these bioactive components in serum and tissues.关键词：ultra-high performance liquid chromatography-quadrupole-orbitrap high resolution mass spectrometry（UHPLC-Q-Orbitrap HRMS）;Yinchen Wulingsan;chemical constituents;constituents absorbed into serum;tissue distribution;famous classical formulas92|34|0更新时间：2026-05-15
- 摘要：Through consulting the ancient and modern literature， this paper made a textual research on the name， origin， producing area， quality evaluation， harvesting time， processing methods and other aspects of Chaenomelis Fructus（CF）， which provides reference and basis for the development and utilization of the famous classical formulas containing CF. The results show that the herbs of the ancient materia medica have mostly used CF as the proper name and taken the fruits into medicine， though it has also been known by other names such as Tiejiaoli， Tiegeng Haitang， and Mutaozi. The original plant of CF in the past dynasties has always been deemed to be Chaenomeles speciosa， family Rosaceae（Flora of China， Zhoupi Mugua）. However， there have also been instances where C. sinensis（known as Mugua in Flora of China and commonly referred to as Guangpi Mugua）， another species of the same family， was inadvertently included in medicinal use. Historically， Xuancheng in Anhui province was regarded as the premier production region. In modern times， the Chunmugua produced in Chun'an， Zhejiang， and the Zimugua produced in Ziqiu， Hubei， have also been recognized for their excellent quality， forming the three genuine producing areas. Since modern times， it is concluded that the quality is the best with firm texture， thick flesh， purplish-red color， and sour taste. The harvesting methods in the past dynasties were to harvest in August of the lunar calendar， the primary processing method of CF was sliced with a copper knife and then sun-dried in ancient documents. According to modern literature， the primary processing method is mainly vertical cutting and sun-drying after harvesting， or scalding in boiling water until gray-white and sun-drying. The processing method was mainly milk steaming before the Ming dynasty and direct steaming after the Ming dynasty. Today， it is typically processed by moistening or steaming into slices， followed by drying， and used as the raw products， or lightly stir-fried before use. The nature， properties， and meridian tropism of CF have evolved from the description of sour， warm and non-toxic in Mingyi Bielu from the Wei and Jin dynasties to sour and warm in the 2025 edition of the Pharmacopoeia of the People's Republic of China. Its toxicity has shifted from the early widespread belief that it was non-toxic to the Ming dynasty text Jiuhuang Bencao， which first documented adverse effects such as excessive consumption damaging the teeth and tendons. Its therapeutic effects have evolved from early indications for damp-bi syndrome， cholera， and nausea to modern uses for relaxing tendons and activating meridians， as well as harmonizing the stomach and transforming dampness. Based on the results of this study， it is recommended that when developing famous classical formulas and health products using CF as the main raw material， C. speciosa should be used as the base material， and it is further recommended that the corresponding processing specifications be selected in accordance with the requirements indicated in the formula， and raw products are recommended to be used as medicine if no processing requirements are indicated.关键词：famous classical formulas;Chaenomelis Fructus;herbal textual research;origin;geoherbalism change;quality evaluation;harvesting and processing91|40|0更新时间：2026-05-15
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Analysis of Mechanism of Active Components of Traditional Chinese Medicine in Treatment of Obesity AI导读
摘要：Obesity refers to a disease characterized by abnormal or excessive fat accumulation that exerts adverse effects on health. It has attracted significant attention due to the health issues and life inconveniences for the patients caused by the disease itself， as well as the life-threatening risks posed by its complications. In recent years， with the increasing incidence of obesity and the gradual decrease in the age of onset， the National Health Commission of the People's Republic of China has launched a three-year "weight management year" campaign to manage the weight of Chinese citizens and reduce the obesity rate. Currently， although there are therapeutic drugs for obesity in clinical practice， their side effects have also aroused widespread concern. Traditional Chinese medicine， with its characteristics of multi-components and multi-targets， plays a crucial role in the treatment of obesity. There are early records in ancient medical classics about the treatment of obesity by using traditional Chinese medicine， and modern clinical studies have also shown that traditional Chinese medicine has a good therapeutic effect on obesity. Studies indicate that the effect of traditional Chinese medicine in improving obesity involves multiple mechanisms. This study took the active components of traditional Chinese medicine as the entry point， sorted out the currently reported active components that can improve obesity， and summarized their preclinical studies， clinical applications， and action mechanisms in the treatment of obesity. At the same time， it pointed out the shortcomings in the current studies and proposed new directions for the study and development based on the current studies. It is expected to provide a theoretical basis for the development of new drugs and products for the treatment of obesity， and at the same time provide bases and new ideas for further studies on the mechanism of obesity.关键词：traditional Chinese medicine;active component;obesity150|46|0更新时间：2026-05-15 - 摘要：Diabetic ulcer （DU） is one of the severe complications of diabetes and affects patients' quality of life. Studies have demonstrated that mitochondrial autophagy plays a critical role in maintaining cellular metabolic homeostasis and injury repair， and its dysfunction is closely associated with the occurrence and progression of DU. In traditional Chinese medicine （TCM）， DU is classified into the category of immersion sores， and its core pathogenesis is "excessive heart fire transferring to the small intestine， leading to damp-heat accumulation in the skin". This theory was founded in Huangdi Neijing， clinically transformed in Jingui Yaolue and further improved by physicians of later generations， forming a dynamic transmission system of "excessive heart fire - transferring to the small intestine - damp-heat steaming - toxin stagnation in the skin"， which is highly consistent with the modern medical regulatory network of mitochondrial autophagy in mechanism. This paper reviews the theoretical origin of the pathogenesis of heart fire and damp-heat and its evolution in diabetic ulcer， and deeply elucidates the internal correlation between them： "excessive heart fire" corresponds to excessive reactive oxygen species production and aggravated oxidative stress induced by high glucose， which is the main inducement of mitochondrial autophagy disorder； "damp-heat in the small intestine" is related to Gut microbiota dysbiosis， skin-gut axis imbalance and energy metabolism disorder， which is a derivative factor blocking autophagic flux. The two factors synergistically lead to the collapse of the mitochondrial quality control system and ultimately result in impaired healing of DU. On this basis， TCM intervention with "clearing heart fire and draining dampness-toxicity" as the core can promote wound healing by regulating mitochondrial autophagy-related pathways through Chinese herbal monomers and compound prescriptions. It provides a new theoretical basis and research idea for the precise integrated diagnosis and treatment of DU with traditional Chinese and western medicine. Further multi-center clinical studies and mechanistic verification are needed to promote the modern transformation of classic TCM theories.关键词：diabetic ulcer;immersion sores;heart fire and damp-heat;mitophagy;gut microbiota102|46|0更新时间：2026-05-15
- 摘要：Atrial fibrillation （AF） is a clinically common arrhythmia， and its pathogenesis and progression is closely associated with metabolic syndrome （MS）. MS is markedly characterized by central obesity， disorders of glucose and lipid metabolism， and hypertension， all of which significantly elevate the risk of AF. The comorbid state of AF and MS is increasingly prevalent in clinical practice. These two conditions pathologically reinforce each other， creating a vicious cycle that substantially increases therapeutic difficulty and the risk of cardiovascular events. Currently， modern medicine lacks comprehensive treatment strategies targeting the common pathological links in AF comorbid with MS.Based on the holistic view of traditional Chinese medicine （TCM） and the concept of "treating different diseases with the same method，" this article systematically constructs， for the first time， a dynamic pathogenesis progression framework for AF comorbid with MS centered on "Deficiency （Xu）， Stagnation （Yu）， Phlegm （Tan）， and Blood Stasis （Yu）". It proposes that the core pathogenesis evolution follows the pattern of "deficiency-induced stagnation， stagnation-induced phlegm generation， and intermingled of phlegm and blood stasis". This process can be summarized into four specific stages： （1） "Deficiency and impediment as the foundation and dysfunction of Qi transformation" is the root of onset， originating from spleen-stomach deficiency， debility of Qi transformation， and malnourishment of the heart. （2） "Stagnation of Qi movement and dysfunction of the pivot mechanism" marks the gradual progression， representing the crucial turning point where the condition shifts from deficiency to excess. （3） "Internal accumulation of dampness-phlegm， ascending disturbance and collaterals obstruction" constitutes the key to pathology， where dampness-phlegm disturbs the heart-mind and obstructs the meridians and collaterals， directly triggering metabolic disorders and palpitations. （4） "Intermingling of phlegm and blood stasis， deep lurking of pathogenic yin forming a stubborn illness"， where phlegm and stasis bind and deposit in the heart meridians， leading to atrial remodeling and the formation of an AF-vulnerable substrate.Based on this pathogenesis framework， this article proposes corresponding therapeutic principles： Treating the fundamental deficiency by "strengthening the middle jiao and nourishing the heart to restore normal pulse"； relieving Qi stagnation by "promoting Qi flow， dispersing constraint， and restoring pivot function" to intercept the pathway of progression； clearing phlegm-turbidity by "resolving dampness， dispelling phlegm， directing counterflow downward， and calming the heart" to eliminate the pathogen disturbing the heart-mind； and breaking blood stasis and masses by "unblocking impediment， resolving blood stasis， softening hardness， and relaxing the meridians" to resolve the deep-seated stubborn illness in the meridians and collaterals. The aim is to provide a new perspective for the clinical treatment of AF comorbid with MS.关键词：atrial fibrillation;metabolic syndrome;deficiency81|32|0更新时间：2026-05-15
- 摘要：Cerebral small vessel disease （CSVD） is a chronic vascular disease affecting the small blood vessels in the brain and the surrounding brain parenchyma. Its pathological mechanisms are complex， and specific therapies are still lacking. Mitophagy， as a key quality control mechanism for maintaining intracellular homeostasis， plays a significant role in the pathogenesis and progression of CSVD， with its dysfunction being a critical factor. The traditional Chinese medicine theory of "Qi deficiency with stagnation" profoundly explains the dynamic pathogenesis of diseases characterized by deficiency leading to excess and the intermingling of deficiency and excess. It closely aligns with the fundamental deficiency and superficial excess nature of CSVD. This article systematically integrates the "Qi deficiency with stagnation" theory with the concept of mitophagy to explore its pathogenic implications in CSVD. It posits that "deficient Qi" （primarily primordial Qi deficiency） is the root cause of the disease， corresponding to impaired cellular energy metabolism and inadequate initiation of mitophagy. "Stagnation" （primarily phlegm and blood stasis obstruction） represents the manifestation of the disease， corresponding to the vicious cycle of accumulated damaged mitochondria， burst of reactive oxygen species and neuroinflammation resulting from dysfunctional autophagy. Based on this， the fundamental therapeutic principle of "tonifying deficiency to unblock stagnation" is proposed， with the core approach being "to replenish Qi and fortify the primordial to restore the foundation of mitophagy， and to invigorate blood and resolve phlegm to unblock the stagnation of mitophagy". By leveraging the multi-component， multi-target holistic regulatory effects of traditional Chinese medicine， this strategy aims to restore mitophagy homeostasis and improve neurovascular unit function， thereby providing a new theoretical basis and therapeutic approach for the integrated prevention and treatment of CSVD with traditional Chinese and Western medicine.关键词：cerebral small vessel disease;Qi deficiency with stagnation;mitophagy;traditional Chinese medicine treatment;theoretical exploration82|36|0更新时间：2026-05-15
- 摘要：Epilepsy（EP） is a chronic neurological disorder caused by abnormal synchronous discharges of neurons. Currently， most patients primarily rely on antiepileptic drugs for treatment. While effective， these medications carry significant side effects and require long-term or even lifelong administration， severely impacting quality of life and imposing a persistent economic burden. Therefore， further elucidating the pathogenesis of EP and the antiepileptic mechanisms is of great significance for developing safer and more effective therapeutic strategies. With the holistic regulatory advantage of synergistic effects via "multi-component， multi-target， and multi-pathway" modes， traditional Chinese medicine（TCM）exhibits great potential in inhibiting neuroinflammation and apoptosis by modulating EP-related signaling pathways. By reviewing relevant literature from Chinese and English databases over the past decade， this paper provides a systematic review of the key signaling pathways involved in the pathogenesis and progression of EP， as well as the regulatory effects of TCM formulas and individual active ingredients on these pathways. Research findings indicate that multiple signaling pathways， including mammalian target of rapamycin（mTOR）， mitogen-activated protein kinase（MAPK）， nuclear factor-κB（NF-κB）， cyclic adenosine monophosphate（cAMP）， phosphoinositide 3-kinase/protein kinase B（PI3K/Akt）， Wnt/β-catenin， and adenosine monophosphate-activated protein kinase（AMPK） play central roles in regulating pathological processes such as neuronal excitability， synaptic plasticity， neuroinflammation， oxidative stress， apoptosis， and autophagy. These pathways constitute the crucial molecular basis for epilepsy development. Multiple TCM formulas（such as Chaihu Longgu Mulitang， Chaibei Zhixiantang， and Jiawei Chaihu Shugantang） and active components（such as curcumin， gastrodin， and tanshinone ⅡA） can effectively inhibit abnormal neuronal discharges， mitigate neuroinflammation and oxidative stress damage， and reduce neuronal apoptosis by targeting these pathways， thereby exerting neuroprotective and antiepileptic effects. This review systematically combs the mechanism of TCM in multi-pathway synergistic regulation， finding that its effect is mainly reflected in the regulation of neuroinflammation-related signaling pathways， with the core mechanism involving the coordinated inhibition of the neuroinflammation pathway centered on the NF-κB signal， and the linked regulation of key pathways such as PI3K/Akt/mTOR and AMPK that involve cell apoptosis and metabolism. This provides a theoretical basis for explaining the pathological process of EP and the mechanism of TCM intervention， and also offers new ideas and directions for the modern research on the prevention and treatment of EP with TCM.关键词：epilepsy;neuroinflammation;signaling pathways;traditional Chinese medicine;active ingredients;mechanism;research progress74|34|0更新时间：2026-05-15
- 摘要：Atherosclerosis （AS） is a chronic cardiovascular disease that poses a serious threat to global health， with persistently high incidence， disability， and mortality rates， making its prevention and treatment increasingly challenging. The pathogenesis of AS is complex， involving multiple pathological processes such as inflammatory responses， lipid metabolism disorders， and endothelial injury， while its underlying cellular and molecular mechanisms remain incompletely elucidated. Programmed cell death （PCD） is an active cell death process triggered by specific signals or stimuli to maintain homeostasis. Modern medical research has demonstrated that dysregulation of various PCD modalities—including apoptosis， pyroptosis， necroptosis， autophagy， ferroptosis， PANoptosis， cuproptosis， and disulfidptosis—is closely associated with the pathogenesis and progression of AS. Elucidating the molecular mechanisms of PCD in AS may provide novel perspectives for understanding， preventing and treating this disease. Traditional Chinese medicine （TCM）， characterized by its multi-target and holistic regulatory approach， has yielded significant achievements in recent studies targeting PCD modulation for AS treatment. TCM compounds exhibit unique advantages in regulating apoptosis， pyroptosis， autophagy， and ferroptosis by intervening in key signaling pathways such as nod-like receptor protein 3（NLRP3）/cysteine aspartate-specific protease-1（Caspase-1）， Nrf2/GPX4， and phosphatidylinositol-3-kinases（PI3K）/protein kinase B（Akt）/mammalian target of rapamycin（mTOR）. The review systematically summarizes the molecular mechanisms of PCD in AS and synthesizes foundational and clinical research from the past five years on TCM compounds targeting PCD for AS intervention， aiming to provide new insights and theoretical foundations for the clinical management and further investigation of AS.关键词：programmed cell death;atherosclerosis;traditional Chinese medicine compound;apoptosis;pyroptosis103|43|0更新时间：2026-05-15
- 摘要：Wilson disease （WD） is an autosomal recessive inherited disorder of copper metabolism that is caused by mutations in the ATP7B gene. Its clinical manifestations include liver damage， neurological impairments， and various non-motor symptoms. Its pathogenesis is highly complex， primarily involving pathological processes such as dysregulated copper metabolism， ferroptosis， autophagy， disrupted iron metabolism， gut microbiota dysbiosis， and cuproptosis. The First Affiliated Hospital of Anhui University of Chinese Medicine has achieved internationally leading expertise in both basic and clinical research on WD. Gandou Fumu decoction （GDFMD） formulated by Professor YANG Wenming， functions in a multi-component， multi-target， and multi-pathway manner. This article systematically reviews the recent advances in the mechanism studies of GDFMD in treating WD. It demonstrates that GDFMD can alleviate liver damage through multiple pathways， including improving lipid metabolism by regulating the peroxisome proliferator-activated （PPAR） signaling pathway， inhibiting ferroptosis mediated by the glutathione peroxidase 4 （GPX4）/acyl coenzyme A synthetase long-chain family， member 4 （ACSL4）/arachidonate-15-lipoxygenase （ALOX15） pathway， modulating autophagy related to phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） and miR-29b-3p/UNC-51-like kinase 1 （ULK1）， blocking the transforming growth factor （TGF）-β1/Smad pro-fibrotic signaling， restoring oxidative/anti-oxidative balance， regulating the gut microbiota， inhibiting c-Jun N-terminal kinase （JNK）-mediated apoptosis， and intervening in cuproptosis. In addition， GDFMD can alleviate kidney damage and swallowing dysfunction and regulate c-fos expression to alleviate brain injury. In summary， GDFMD demonstrates multi-dimensional pharmacological activities in the treatment of WD， showing broad prospects for clinical application and future research.关键词：Gandou Fumu decoction （GDFMD）;Wilson disease;mechanism;research progress100|46|0更新时间：2026-05-15
- 摘要：Pulmonary hypertension （PH） is a chronic progressive disease that can lead to right heart failure and even death. Its clinical manifestations are mainly dyspnea， chest pain， and chest tightness， which seriously affect patients quality of life. Currently， effective pharmacological treatments are lacking. Studies have shown that the occurrence and development of PH are closely related to programmed cell death （PCD） mechanisms， including autophagy， pyroptosis， apoptosis， ferroptosis， cuproptosis， and disulfidptosis. Clarifying the molecular mechanisms of PCD in PH and thoroughly investigating cellular signaling pathways and PCD-related targets are of great significance for the prevention and treatment of PH. In recent years， traditional Chinese medicine （TCM） has played an important role in the treatment of PH. A relatively large number of mechanistic studies have explored the treatment of PH with TCM at the level of PCD， and have found that some TCM monomers and compound formulas can regulate signaling pathways to prevent and treat PH. This article reviews recent research progress on the basic molecular mechanisms of various types of PCD， the association between PCD and PH， and key targets and pathways through which TCM treats PH via PCD regulation. Current evidence suggests that TCM plays an important role in the prevention and treatment of PH through the regulation of PCD. Numerous mechanistic and experimental studies have been conducted worldwide， confirming that TCM monomers such as cantharidin and puerarin， as well as compound formulas such as Qihong Bufei decoction and Feixin decoction， can intervene in PH by regulating PCD-related signaling pathways. These findings provide a reference basis and practical guidance for the clinical treatment of PH.关键词：pulmonary hypertension;programmed cell death;mechanism research;traditional Chinese medicine;research progress84|41|0更新时间：2026-05-15
- 摘要：Diabetic atherosclerosis（DM-AS） is the pathological basis of diabetic macrovascular complications and is a major cause of cardiovascular events in patients with diabetes. Persistent hyperglycemia can damage the vascular endothelium and exacerbate lipid metabolic disorders and inflammatory responses， promoting the transition of plaques from formation to vulnerability， thereby increasing the risk of rupture and thrombosis. Therefore， maintaining plaque stability is of great importance for the prevention of cardiovascular events. The degree of macrophage foam cell formation and the imbalance between pro-inflammatory M1 polarization and anti-inflammatory reparative M2 polarization directly affect plaque stability. Autophagy is a key pathway for maintaining macrophage homeostasis. By regulating lipid metabolism， inflammation-related signaling， and autophagic flux， autophagy influences the inflammatory burden of plaques and the expansion of the necrotic core， thereby contributing to plaque stabilization. Traditional Chinese medicine（TCM） has the advantages of multi-component， multi-target， and holistic regulation. Previous studies showed that active compounds derived from Chinese materia medica and TCM formulas exhibit notable advantages in modulating the autophagy network and intervening in the progression of DM-AS plaques. Focusing on macrophage autophagy， this review systematically summarizes the mechanisms by which key pathways， including adenosine monophosphate-activated protein kinase/mammalian target of rapamycin（AMPK/mTOR）， phosphoinositide 3-kinase/protein kinase B（PI3K/Akt）， peroxisome proliferator-activated receptor（PPAR）， and receptor for advanced glycation end-product/nuclear factor-κB（RAGE/NF-κB）， target macrophage autophagy to mediate polarization balance and exert effects at different stages of DM-AS. It also summarizes current research on TCM compounds and formulas that regulate autophagy and thereby inhibit plaque progression， with the aim of providing new insights for mechanistic studies and clinical translation in DM-AS.关键词：diabetes;atherosclerosis;macrophage autophagy;macrophage polarization;plaque stability;signaling pathway;traditional Chinese medicine93|42|0更新时间：2026-05-15
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