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- 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 days 0， 5， 10， and 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 days 3， 6， and 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;rehabilitation11|8|0更新时间：2026-04-29
- 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 repair8|9|0更新时间：2026-04-29
- 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 fibrosis8|10|0更新时间：2026-04-29
- 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）7|10|0更新时间：2026-04-29
- 摘要：Digestive system malignant tumors （DTs） are one of the leading causes of death globally and carry a heavy economic burden. Gut microbiota plays a critical role in maintaining host health， including providing nutrition， defending against pathogens， and promoting immune development. In recent years， more and more studies have shown that dysbiosis of gut microbiota is closely associated with DTs such as gastric cancer， liver cancer， and colon cancer. Therefore， targeted regulation of gut microbiota plays a potential role in inhibiting the growth and metastasis of DTs， while its specific regulatory mechanism remains unclear. As the studies about the anti-tumor effects of traditional Chinese medicine （TCM）， especially the basic and clinical studies on the regulation of gut microbiota by TCM in tumor treatment， have been growing， the therapeutic effects of TCM on DTs have attracted much attention. This paper provides a systematic review of the relationship between gut microbiota and DTs， as well as the related studies on the modulation of gut microbiota by TCM against DT， with the aim of providing a foundation and direction for future basic and clinical studies on DTs. The literature review shows that gut microbiota influence the occurrence and development of DTs through multiple pathways. These pathways include triggering chronic inflammation， producing oncogenic metabolites， inducing genomic instability， regulating the immune system， and altering the tumor microenvironment. TCM can exert anti-DT effects by regulating the composition of gut microbiota， modulating gut microbiota metabolites， repairing intestinal barrier function， and influencing immune functions. Therefore， understanding the relationship between gut microbiota and DTs and the regulatory mechanisms of TCM may provide new strategies for future prevention and treatment of DTs.关键词：gut microbiota;digestive system malignant tumors;traditional Chinese medicine;immunity;metabolite regulation6|3|0更新时间：2026-04-29
- 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;depression11|10|0更新时间：2026-04-29
- 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 inhibitor8|3|0更新时间：2026-04-29
- 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）9|5|0更新时间：2026-04-29
- 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 and heart index， 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， P<0.01）. 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）. 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 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 metabolism23|9|0更新时间：2026-04-29
- 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 Decoction （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 review10|5|0更新时间：2026-04-29
- 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 NLRP3/Caspase-1， Nrf2/GPX4， and PI3K/Akt/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;pyroptosis5|10|0更新时间：2026-04-29
- 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 microbiota4|11|0更新时间：2026-04-29
- 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 progress8|10|0更新时间：2026-04-29
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Mechanism of Ursodeoxycholic Acid in Ameliorating Hyperlipidemia and Atherosclerosis in ApoE-/- Mice
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 （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 disorders6|9|0更新时间：2026-04-29 - 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 （P<0.05， P<0.01） 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 （P<0.05）， 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 synthesis10|10|0更新时间：2026-04-29
- 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 pathway6|9|0更新时间：2026-04-29
- 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;inflammation11|9|0更新时间：2026-04-29
- 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;obesity8|9|0更新时间：2026-04-29
- 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 theory4|6|0更新时间：2026-04-29
- 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 treatment8|6|0更新时间：2026-04-29
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