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- 摘要：Neuropathic pain （NP） is a chronic pain syndrome resulting from injury， inflammation， or dysfunction of the somatosensory nervous system. Its pathogenesis is complex and intimately associated with peripheral sensitization and maladaptive neuroplasticity within the central nervous system. The core clinical manifestations， including spontaneous pain， allodynia， and paresthesia， severely compromise patients’ quality of life and pose substantial challenges to clinical management. Endoplasmic reticulum stress （ERS）， a critical cellular defense mechanism against disrupted intracellular homeostasis， is primarily initiated and modulated through three canonical branches of the unfolded protein response （UPR）： the protein kinase RNA-like endoplasmic reticulum kinase （PERK） pathway， the inositol-requiring transmembrane kinase/endonuclease 1α （IRE1α） pathway， and the activating transcription factor 6 （ATF6） pathway. These signaling cascades play a pivotal role in the pathological progression of NP. Traditional Chinese medicine （TCM） exhibits unique advantages in the treatment of NP. Leveraging its hallmark characteristics of multi-target， multi-pathway， and holistic regulation， TCM can systematically modulate the ERS signaling network to inhibit neuronal apoptosis， attenuate neuroinflammatory infiltration， and rectify autophagic dysfunction， ultimately promoting the repair and regeneration of damaged neural tissue. This review systematically summarizes the core role of ERS in the occurrence and development of NP. It focuses on the latest research progress regarding ERS pathway modulation in NP amelioration by representative TCM interventions， including potential core bioactive components （e.g.， tanshinoneⅡA， catalpol， and formononetin）， classic and empirical compound formulas （e.g.， Huangqi Guizhi Wuwu decoction， Compound Qiying granules， and Tangluoning）， and TCM external therapies （e.g.， electroacupuncture， moxibustion with seed-sized moxa cone， and acupotomy）. Through an in-depth analysis of the functional characteristics and mechanisms of these TCM interventions， particularly their bidirectional regulation and multi-target synergy， this review aims to provide a solid theoretical foundation for further optimizing TCM-based strategies for NP prevention and treatment and to delineate future directions for clinical translation of related research achievements and targeted drug development.关键词：endoplasmic reticulum stress;neuropathic pain;research progress;traditional Chinese medicine;mechanism3|0|0更新时间：2026-07-10
- 摘要：ObjectiveTo systematically identify the main chemical components of Linggui Zhugan granules （LGZGG）， and to explore the pharmacodynamic substance basis for the treatment of metabolic dysfunction-associated steatohepatitis （MASH）.MethodsThe chemical components of LGZGG were systematically analyzed by ultra-performance liquid chromatography-quadrupole-time-of-flight tandem mass spectrometry （UPLC-Q-TOF-MS/MS）. The protein-protein interaction （PPI） network and "compound prescription-disease-component-target" network were constructed by network target analysis to predict the potential pharmacodynamic substances and core targets of LGZGG in the treatment of MASH. The potential pharmacodynamic substances were enriched by macroporous adsorption resin， and the chemical composition of the LGZGG-50% ethanol elution fraction （LGZGG-50） was analyzed by UPLC-Q-TOF-MS/MS. The mouse model of MASH was established by feeding a high-fat， high-cholesterol， and high-fructose diet for 12 weeks. Mice were randomly allocated into normal， model， positive drug （MGL-3196， 1 mg·kg-1）， LGZGG （crude drug， 34 g·kg-1·d-1）， LGZGG-50 （crude drug， 34 g·kg-1·d-1） groups. The levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， and high-density lipoprotein cholesterol （HDL-C） in the serum were measured， and the pathological changes in the liver tissue were observed by hematoxylin-eosin （HE） and Sirius red staining. The in vivo efficacy of LGZGG and LGZGG-50 in the treatment of MASH was evaluated on the basis of the findings. The expression levels of adenosine monophosphate-activated protein kinase （AMPK）， phosphorylated AMPK （p-AMPK）， silent information regulator 2-related enzyme 1 （SIRT1）， peroxisome proliferator-activated receptor α （PPARα）， and carnitine palmitoyltransferase 1A （CPT1A） in the liver tissue were determined by Western blot to verify the regulatory effects of core targets.ResultsA total of 83 chemical components were identified from LGZGG， including 20 flavonoids， 13 terpenoids， 17 organic acids， 7 amino acids， 11 glycosides， 3 nucleosides， 3 aromatics， 3 alkaloids， 2 phenylpropanoids， 2 sugars， 1 nucleic acid， and 1 steroid. A total of 134 common targets were obtained by network target analysis. The core targets included SIRT1， PPARα， nuclear factor-kappa B subunit 1 （NFκB1）， and interleukin-6 （IL-6）. Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analysis revealed that the targets were mainly enriched in the AMPK， PPAR and other signaling pathways. The topological analysis of the "compound prescription-disease-component-target" network showed that the potential pharmacodynamic substances of LGZGG against MASH were flavonoids and terpenoids. The relative content of flavonoids and terpenes in LGZGG-50 were 74.00% and 62.41% in positive and negative ion modes， respectively， indicating that LGZGG-50 effectively enriched total flavonoids and total terpenoids. The results of in vivo efficacy showed that compared with the model group， LGZGG and LGZGG-50 reducef the body weight， liver weight， serum TG， GLU， and ALT levels of MASH mice （P0.05）， and LGZGG additionally increased the HDL-C level （P0.05）. Both groups alleviated the pathological damage in the liver tissue. The results of Western blot showed that compared with the model group， the protein levels of p-AMPK/AMPK， SIRT1， PPARα， and CPT1A were up-regulated in the LGZGG group （P0.05）， and those of p-AMPK/AMPK and CPT1A were up-regulated in the LGZGG-50 group （P0.05）.ConclusionLGZGG ameliorates MASH， with the main pharmacodynamic substances being flavonoids and terpenoids. The mechanism may be related to the regulation of AMPK/SIRT1/PPARα signaling pathway， improvement of lipid metabolism， and alleviation of pathological damage in the liver tissue.关键词：Linggui Zhugan granules;chemical component;identification;metabolic dysfunction-associated steatohepatitis;ultra-performance liquid chromatography-quadrupole-time-of-flight tandem mass spectrometry （UPLC-Q-TOF-MS/MS）2|0|0更新时间：2026-07-10
- 摘要：Digestive system tumors are the leading cause of cancer incidence and mortality globally， and their occurrence and development generally follow the key pathological process of inflammation-cancer transformation. Therefore， intervening in the precancerous lesion stage is an important strategy to block malignant transformation of the disease and reduce the incidence rate of tumors. Banxia Xiexin Tang-related prescriptions （including Banxia Xiexin Tang， Shengjiang Xiexin Tang， and Gancao Xiexin Tang） originated from the Shanghan Zabinglun They follow the principle of pungent dispersing and bitter descending， combination of cold and warm medicinals， and tonifying deficiency and purging excess， which aligns with the core pathogenesis of digestive system precancerous lesions characterized by cold-heat intermingling and disorder of ascending and descending. These prescriptions are widely used in the clinical treatment of various digestive system inflammatory disorders such as atrophic gastritis， ulcerative colitis， and reflux esophagitis. This review systematically summarizes the theoretical basis， clinical evidence， and therapeutic mechanisms of such prescriptions in preventing and treating the inflammation-cancer transformation process in the digestive system. Clinical studies have shown that whether used alone or in combination with modern therapies， Banxia Xiexin Tang can effectively alleviate symptoms， repair histopathological changes， and improve patients' quality of life. Basic research further reveals that their efficacy stems from multi-target systemic regulatory effects： ameliorating the chronic inflammatory microenvironment， antagonizing oxidative stress， reshaping the gut microbiota， restoring the immune balance， regulating cell proliferation and apoptosis， etc. On the basis of the convergence of traditional Chinese and Western medicine understanding of inflammation-cancer transformation， this article constructs a research framework centered on regulating the inflammatory microenvironment homeostasis to systematically elucidate the mechanism of treating different diseases with the same method （Banxia Xiexin Tang）. In view of the limitations of current research in terms of evidence level， disease-syndrome combination models， and overall mechanism analysis of compound prescriptions， this article proposes future research directions of integrating high-quality clinical research， systems biology， and cutting-edge technologies， providing a new theoretical basis and translational ideas for the precise prevention and control of digestive system tumors with traditional Chinese medicine.关键词：Banxia Xiexin Tang-related prescriptions;digestive system;inflammation-cancer transformation;mechanism study;clinical study3|0|0更新时间：2026-07-10
- 摘要：ObjectiveTo investigate the platelet metabolomic characteristics of the rat model of coronary heart disease （CHD） with blood stasis syndrome （BSS） based on ultra-high performance liquid chromatography coupled with quadrupole-Orbitrap high-resolution mass spectrometry （UPLC-Q-Exactive Orbitrap-MS）， screen potential biomarkers and metabolic pathway information， and elucidate the association mechanism between platelet metabolic disorders and myocardial injury.MethodsA total of 12 rats were randomized into a normal group and a modle group. The rat model of CHD-BSS was established by continuous high-fat feeding， intragastric administration of vitamin D3 in divided doses combined with subcutaneous injection of isoproterenol. Additionally， changes in standard lead Ⅱ electrocardiogram （ECG） and myocardial histopathological alterations of rats in the two groups were observed to evaluate myocardial injury in the modle group. After preprocessing of the untargeted metabolomic data of platelet samples from the two groups， multivariate statistical analysis and differential screening were performed sequentially. Principal component analysis （PCA） was performed to verify the separation of metabolic profiles of samples between groups. An orthogonal partial least squares-discriminant analysis （OPLS-DA） model was then constructed to preliminarily screen potential differential metabolites based on model parameters. Secondary screening was conducted with the fold change of metabolite expression to finally identify metabolites with significant intergroup differences， and metabolic pathway enrichment analysis was carried out based on these differential metabolites. Finally， potential platelet-specific biomarkers were identified based on receiver operating characteristic（ROC） curves.ResultsCompared with the normal group， the modle group presented obvious elevation of the J point and an ST-segment elevation greater than 0.1 mV on ECG， as well as pathological injuries such as loose arrangement of fibers and cellular vacuolar degeneration in the myocardial tissue. A total of 370 differentially expressed metabolites were dysregulated in the modle group， involving 8 significantly enriched metabolic pathways，such as purine metabolism， arachidonic acid metabolism， oxidative phosphorylation and adenosine monophosphate-activated protein kinase （AMPK） signaling pathway. Nine differential metabolites enriched in these pathways showed statistically significant differences in content. ROC curve analysis revealed that the area under the curve（AUC） of all characteristic metabolites was higher than 0.8. Among them， the AUC values of four metabolites， including sphinganine 1-phosphate， sphingosine 1-phosphate， 12-ketoleukotriene B4 and 14，15-dihydroxyeicosatrienoic acid， reached 1.0， indicating their potential as biomarkers.ConclusionPlatelet metabolic characteristics are significantly altered in the rat model of CHD-BSS. The screened potential biomarkers possess favorable diagnostic performance. The pathological changes mediated by these metabolites， including inflammatory response， thrombosis， and energy metabolism disorders， serve as critical mechanisms for abnormal platelet activation and subsequent myocardial injury. Platelet metabolomics provides a new perspective for the screening of biomarkers and research on pathological mechanisms of CHD-BSS.关键词：coronary heart disease;blood stasis syndrome;platelets;metabolomics;biomarker;myocardial injury2|0|0更新时间：2026-07-10
- 摘要：Malignant tumors are major diseases with a high incidence worldwide and seriously threaten human health， and their occurrence and development are closely associated with the abnormal activation of multiple signaling pathways. Among them， the vascular endothelial growth factor （VEGF）/VEGF receptor （VEGFR） signaling pathway plays a key regulatory role in tumor angiogenesis， which can be widely implicated in tumor proliferation， invasion， and metastasis through regulating the expression of downstream signaling proteins and genes， serving as a key target for cancer targeted therapy. Traditional Chinese medicine （TCM） possesses unique advantages including multiple components， multiple targets， holistic regulation， and mild adverse reactions in cancer prevention and treatment. This paper systematically sorts out existing research findings and analyzes the anti-tumor mechanisms of TCM in modulating this signaling pathway. Furthermore， this paper summarizes that TCM active components （such as oxymatrine， quercetin， and celastrol）， extracts （such as Prunellae Spica extract and Cinnamomi Cortex extract）， and compound prescriptions （such as Yupingfeng San and modified Wenyang Sanjie Formula） can inhibit tumor angiogenesis， reverse epithelial-mesenchymal transition， improve the tumor microenvironment， promote cancer cell apoptosis， and suppress cancer cell proliferation， migration， and invasion by regulating the VEGF/VEGFR signaling pathway and its key molecules， thereby exerting anti-tumor effects. This review provides new ideas for the research and development of cancer drugs and the optimization of treatment regimens.关键词：vascular endothelial growth factor （VEGF）/VEGF receptor （VEGFR） signaling pathway;cancer;traditional Chinese medicine （TCM） active component;TCM extract;TCM compound prescription1|0|0更新时间：2026-07-10
- 摘要：ObjectiveTo investigate the synergistic inhibitory effect of chidamide （CHI） combined with compound Kushen injection （CKI） on breast cancer MCF-7 cells and to elucidate the potential molecular mechanisms based on transcriptomics analysis.MethodsCell proliferation was detected by the methyl thiazolyl tetrazolium （MTT） assay， and the "one belt and one line" method was adopted to screen the optimal mass concentration for synergistic effect. According to the combination index （CI） values， cells were allocated into the blank， CHI （1.6 mg·L-1）， CKI （0.4 g·L-1）， and CHI+CKI （1.6 mg·L-1+0.4 g·L-1） groups. Transwell assay was employed to examine cell migration， and flow cytometry to measure cell cycle distribution and apoptosis rate. Transcriptome sequencing （RNA-seq） and weighted gene co-expression network analysis （WGCNA） were performed to screen the key modules highly correlated with the cell inhibition rate. Candidate genes were identified by intersecting module genes with differentially expressed genes （DEGs）， followed by functional enrichment analysis. Western blot was employed to quantify the protein levels of histone deacetylase 1 （HDAC1）， cyclic adenosine monophosphate （cAMP）-dependent protein kinase A （PKA）， cyclin-dependent kinase inhibitor 1 （p21）， cAMP response element-binding protein （CREB） and its phosphorylated form （p-CREB）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in cells of each group.ResultsCompared with the blank group， both CHI and CKI monotherapies inhibited the proliferation of MCF-7 cells in a mass concentration-dependent manner. Compared with the blank and monotherapy groups， CHI+CKI inhibited cell migration， increased the proportion of cells arrested in the G0/G1 phase， and elevated the apoptosis rate （P0.01）. WGCNA identified the MEred module strongly correlated with the inhibition rate （r=0.90， P0.01）， yielding 97 candidate genes upon intersection with DEGs. Kyoto Encyclopedia of Genes and Genomes （KEGG） analysis indicated significant enrichment of the cAMP signaling pathway. Western blot results showed that compared with the blank group， all treatment groups down-regulated the expression of HDAC1， up-regulated the expression of PKA and p21， and increased the p-CREB/CREB and Bax/Bcl-2 ratios （P0.01）. Compared with the monotherapy groups， CHI+CKI further up-regulated the PKA and p21 expression and increased the p-CREB/CREB and Bax/Bcl-2 ratios （P0.01）.ConclusionThe combination of CHI and CKI exerts a significant synergistic anti-tumor effect. CHI exerts epigenetic regulation by inhibiting HDAC1， which， in combination with CKI， may further contribute to the activation of the cAMP/PKA/CREB signaling pathway， leading to up-regulation of p21 expression and the Bax/Bcl-2 ratio， thereby promoting cell cycle arrest and apoptosis.关键词：chidamide;compound Kushen injection;breast cancer;synergism;transcriptomics;cyclic adenosine monophosphate （cAMP） signaling pathway1|0|0更新时间：2026-07-10
- 摘要：ObjectiveTo investigate the protective effect of Notoginseng total saponins （NTS） against doxorubicin （DOX）-induced cardiotoxicity （DIC） and to explore the specific mechanism by which NTS inhibits ferroptosis via the nuclear facor erythroid 2-related factor 2 （Nrf2） signaling pathway.MethodsC57BL/6 mice were assigned into control， DOX （6 mg·kg-1）， low-dose （3 g·kg-1） NTS + DOX （Low NTS+DOX）， high-dose （6 g·kg-1） NTS + DOX （High NTS+DOX）， and dexrazoxane （30 mg·kg-1） + DOX （DEX+DOX） groups （n=10 per group）. On days 6 and 9， other groups except the control group received intravenous injections of DOX. The control group was injected with an equal volume of normal saline （0.9% NaCl） at the same time points. Thirty minutes before each DOX injection， the DEX+DOX group was intravenously administered DEX. The NTS-treated groups received daily oral gavage of NTS dissolved in ultrapure water for 12 days， starting 5 days before DOX administration. The control and DOX groups were administered an equal volume of distilled water by gavage during the same period. Cardiac function was assessed by echocardiography. The myocardial injury was evaluated by hematoxylin-eosin （HE） staining and serum cardiac injury markers. The iron（Ⅱ） ion （Fe2+） level and lipid peroxidation were measured via commercial kits. Apoptosis was observed by terminal deoxygenucleotidyl transferase dUTP nick-end labeling （TUNEL） staining. Nrf2 nuclear translocation and the expression of downstream proteins including nuclear receptor coactivator 4 （NCOA4）， ferroportin （FPN）， glutathione peroxidase 4 （GPX4） and transferrin receptor 1 （TfR1）were examined by immunofluorescence and Western blot.ResultsCompared with the control group， the DOX group showed decreased left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01）， elevated levels of creatine kinase-MB （CK-MB） and lactate dehydrogenase （LDH） （P<0.01）， increased Fe2+ and malondialdehyde （MDA） （P<0.01）， and reduced glutathione （GSH） （P<0.01）. Western blot analysis revealed downregulated expression of Nrf2， FPN， GPX4， and TfR1 （P<0.05， P<0.01）， and upregulated expression of NCOA4 （P<0.01）. Compared with the DOX group， NTS improved LVFS and LVEF （P<0.05， P<0.01）， decreased CK-MB and LDH levels （P<0.01）， lowered Fe2+ and MDA levels （P<0.01）， and increased the GSH level （P<0.05）. At the protein level， NTS enhanced the expression of Nrf2 and GPX4 （P<0.05， P<0.01） and showed a regulatory trend on the expression of FPN， TfR1， and NCOA4， although these changes were not statistically significant.ConclusionNTS can alleviate DOX-induced cardiotoxicity by inhibiting ferroptosis through activation of the Nrf2 signaling pathway.关键词：doxorubicin-induced cardiotoxicity;ferroptosis;Notoginseng total saponins;nuclear facor erythroid 2-related factor 2 （Nrf2）2|3|0更新时间：2026-07-09
- 摘要：ObjectiveTo evaluate the efficacy and safety of Wenyang Jiedu granules combined with conventional Western medicine in the treatment of severe coronavirus disease 2019 （COVID-19）.MethodsA multicenter， open-label， randomized controlled clinical trial was conducted. Eligible patients were randomly divided into the observation group and the control group at a 1∶1 ratio. The control group received conventional Western medicine treatment in accordance with the Diagnosis and Treatment Protocol for COVID-19 （Trial Version 10）. On the basis of conventional Western medicine treatment， the observation group was additionally given Wenyang Jiedu granules， 2 sachets （30 g） each time， three times a day， with a treatment course of 14 days. The primary outcome was the proportion of clinical progression on day 14， and the secondary outcomes included mortality， the proportion of clinical improvement and the the incidence of composite clinical events at day 7， 14 and 28 as well. The prognostic differences were compared between the two groups.ResultsA total of 185 participants were enrolled， including 91 cases in the observation group and 94 cases in the control group. The baseline characteristics were balanced and comparable between the two groups. After excluding 2 incorrectly enrolled cases， 183 patients were included in the modified intention-to-treat （mITT） set； after excluding cases of dropout and protocol violation， 151 patients were included in the per-protocol set （PPS）. The results of both analysis sets showed that the proportion of clinical progression on day 14 in the observation group was significantly lower than that in the control group （mITT： 7.9% vs 18.1%， P=0.041； PPS 4.0% vs 17.1%， P=0.015）. Subgroup analysis indicated that the observation group achieved more obvious efficacy（P<0.05） in patients aged over 60 years ［relative risk （RR）=0.367， 95% confidence interval （95%CI）： 0.143-0.941］， patients with diabetes （RR=0.183， 95%CI： 0.036-0.930）， and patients without chronic respiratory diseases （RR=0.357， 95%CI 0.130-0.981）. Compared with the control group， the observation group had significantly lower incidence of composite clinical events at day 7 （22.5% vs 39.4%， P=0.014） and day 14 （39.3% vs 54.3%， P=0.043）. The mortality at day 7， 14 and 28， the proportion of clinical progression at day 7 and 28， the rate of invasive mechanical ventilation， and the rate of non-invasive mechanical ventilation/high-flow oxygen therapy showed a downward trend， while the proportion of clinical improvement at day 7， 14 and 28 showed an upward trend， without statistically significant differences. There was no significant difference in the incidence of adverse events between the two groups.ConclusionWenyang Jiedu Granules can reduce the risk of disease progression on day 14 in patients with severe COVID-19， with more prominent advantages in patients aged over 60 years， patients complicated with diabetes， and patients without chronic respiratory diseases； It can also reduce the incidence of composite clinical events； and it demonstrates favorable safety profile.关键词：Wenyangjiedu granules;severe coronavirus disease 2019 （COVID-19）;strengthening vital qi to eliminate pathogenic factor;randomised controlled trial;clinical efficacy28|26|0更新时间：2026-06-30
- 摘要：ObjectiveThis paper aims to investigate the effect of Huangqi Guizhi Wuwu Tang combined with low-molecular-weight heparin sodium on preventing deep vein thrombosis of the lower extremities in parturients undergoing cesarean section.MethodsA total of 781 parturients who underwent cesarean section （from June 2022 to October 2025） were included in the study and randomly divided into a control group and an observation group using a random number table method. Two cases were lost to follow-up in this study. The parturients undergoing cesarean section in the control group （389 cases） received low-molecular-weight heparin sodium and a traditional Chinese medicine placebo （similar in color to the traditional Chinese medicine in the observation group）. The parturients in the observation group （390 cases） were treated with Huangqi Guizhi Wuwu Tang in addition to the intervention of the control group. The incidence of deep vein thrombosis of the lower extremities in parturients from both groups undergoing cesarean section， the numerical rating scale （NRS） pain scores on the first day， third day， and seventh day after cesarean section， the venous blood flow velocity in the lower extremities of parturients before and after treatment （popliteal vein， femoral vein）， the venous clinical severity score （VCSS） of parturients in the two groups after treatment， the coagulation function indicators before and after treatment ［prothrombin time（PT），activated partial thromboplastin time （APTT），fibrinogen（FIB），D-Dimer］， hemorheological indicators ［high shear viscosity（HSV），low shear viscosity（LSV），erythrocyte sedimentation rate（ESR）］， and the incidence of adverse reactions were compared.ResultsThe incidence of deep venous thrombosis in the lower extremities of parturients after cesarean section in the observation group （0.77%） was lower than that in the control group （2.83%） （χ2=4.676， P=0.031）. On the first， third， and seventh days after cesarean section， the NRS scores of the parturients in the observation group were lower than those of the control group （t=69.509， 23.266， 90.979； P<0.05 for all）. Before treatment， the venous blood flow velocities （popliteal vein， femoral vein） of the lower extremities in the parturients from the two groups were compared， and no statistical difference was found （P>0.05 for all）. After treatment， the venous blood flow velocities （popliteal vein， femoral vein） of the lower extremities in the parturients from these two groups increased， with higher indicator levels among the parturients in the observation group than those in the control group （t=40.492， 21.587； P<0.05 for all）. After treatment， the scores of each item in the VCSS of parturients were lower in the observation group than those in the control group （t=46.234， 37.786， 69.016， 39.464； P<0.05 for all）. Before treatment， coagulation function indicators （PT， APTT， FIB， and D-Dimer） of the parturients from the two groups were compared， and there was no statistical significance in the differences （P>0.05 for all）. After treatment， PT and APTT increased， while FIB and D-D decreased in the parturients from both groups. The degrees of increase and decrease of all indicators were greater among parturients in the observation group than those in the control group （t=18.916， 12.522， 24.787， 27.635； P<0.05 for all）. Before treatment， the hemorheology indicators （HSV， LSV， ESR） in the parturients from both groups were compared， and there was no statistical significance in the differences. After treatment， these indicators in the parturients from both groups decreased， with lower indicator levels in the observation group than those in the control group （t=85.734， 26.280， 56.792； P<0.05 for all）. The incidence of adverse reactions of parturients after cesarean section in the observation group （3.85%） compared with that in the control group （3.34%）， and there was no statistically significant difference （χ²=0.143， P=0.705）.ConclusionHuangqi Guizhi Wuwu Tang combined with low-molecular-weight heparin sodium demonstrates a favorable preventive effect on deep vein thrombosis of the lower extremities in parturients undergoing cesarean section. This combined regimen improves lower extremity function， alleviates postoperative pain after cesarean section， and enhances lower-extremity blood perfusion in parturients， with safety and reliability.关键词：caesarean section;low-molecular-weight heparin sodium;Huangqi Guizhi Wuwu Tang;deep vein thrombosis of lower extremity;coagulation function;adverse reaction33|25|0更新时间：2026-06-30
- 摘要：Type 2 diabetes mellitus is a common endocrine syndrome characterized by glucose metabolism disorders， often accompanied by lipid metabolism dysfunction and complicated with hyperlipidemia. The etiology of type 2 diabetes mellitus has not been fully elucidated， but insulin resistance and pancreatic β-cell dysfunction play central roles in its pathophysiology. Insulin resistance is the shared pathological basis of these two diseases. An imbalance in insulin function directly disrupts lipid metabolic order， thereby inducing hyperlipidemia. Modern medical treatments primarily target regulating laboratory indicators. While this approach yields certain therapy to some extent， it is associated with unstable efficacy， frequent adverse reactions， and a high recurrence rate， which imposes a heavy burden on patients. In recent years， traditional Chinese medicine has achieved notable progress in the treatment of type 2 diabetes mellitus complicated with hyperlipidemia. Traditional Chinese medicine exhibits distinct advantages， including multi-targeted and multi-pathway actions， simplicity， high efficacy， cost-effectiveness， and minimal side effects in intervening type 2 diabetes mellitus complicated with hyperlipidemia. Numerous studies have demonstrated that traditional Chinese medicine components （e.g.， traditional Chinese medicine-derived extracellular vesicles） and traditional Chinese medicine compound formulae can modulate the signaling pathways related to disease to regulate insulin sensitivity， lipid metabolism， inflammatory responses， endoplasmic reticulum stress， gut microbiota， and energy homeostasis， thereby ameliorating glucose-lipid metabolic disorders and delaying disease progression. Therefore， this review summarized the key signaling pathways targeted by traditional Chinese medicine in intervening type 2 diabetes mellitus complicated with hyperlipidemia， including the insulin receptor substrate/phosphatidylinositol 3 kinase/protein kinase B （IRS/PI3K/Akt） signaling pathway， adenosine monophosphate-activated protein kinase （AMPK） signaling pathway， peroxisome proliferator-activated receptors （PPARs） signaling pathway， the nuclear factor kappa B/c-Jun N-terminal kinase （NF-κB/JNK） signaling pathway， protein kinase RNA-like endoplasmic reticulum kinase （PERK） signaling pathway， the short-chain fatty acid/glucagon-like peptide-1 （SCFAs/GLP-1） signaling pathway， Wingless/Int-1 （Wnt） signaling pathway， the protein kinase C （PKC） signaling pathway， and sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator-1alpha （SIRT1/PGC-1α） signaling pathway， aiming to provide a reference direction for the research and development of novel drugs.关键词：traditional Chinese medicine;type 2 diabetes mellitus;hyperlipidemia;signaling pathway;mechanism of action34|26|0更新时间：2026-06-30
- 摘要：ObjectiveThis paper aims to investigate the action mechanism of betulinic acid （BA） in inhibiting ferroptosis and improving non-alcoholic fatty liver disease （NAFLD） through bioinformatics analysis and experimental validation， providing references for both basic research and clinical applications of NAFLD.MethodsBased on bioinformatics analysis， the NAFLD-related microarray datasets， GSE89632 and GSE63067， were downloaded from the gene expression omnibus （GEO） database. Ferroptosis-related genes were downloaded from the ferroptosis database， and differentially expressed genes （DEGs） related to NAFLD ferroptosis were screened to construct enrichment analyses of protein-protein interaction （PPI） networks， gene ontology （GO）， and Kyoto encyclopedia of genes and genomes （KEGG）. Different algorithms were used to mine key DEGs， which were further analyzed for correlation， immune infiltration， and immune cell differences of key DGEs. Least absolute shrinkage and selection operator （LASSO） regression analysis was conducted to identify disease feature genes from the key DEGs. The intersection of key genes from various algorithms of Cytoscape and the disease feature genes identified through LASSO regression was used to select core genes. The survival curve， namely receiver operating characteristic （ROC） curve， was performed to validate these core genes. Potential new targets for NAFLD were analyzed and predicted， and molecular docking was used to verify the core targets and active components of traditional Chinese medicine. Animal experiment was conducted. Fifty C57BL/6J mice were randomly divided into the normal group， model group， low-dose/high-dose BA groups， and silymarin group. The model was established by feeding a high-fat and high-cholesterol diet combined with 2.5% dextran sulfate sodium （DSS） in drinking water， followed by continuous gavage for 24 days in the drug groups. Body weight and liver index of mice were measured at sampling， and hematoxylin and eosin （HE） staining was used to assess hepatic lipid droplet deposition. Western blot and real-time polymerase chain reaction （real-time PCR） were performed to detect the expression levels of glutathione peroxidase 7 （GPX7）， lactotransferrin （LTF）， S100 calcium binding protein A8 （S100A8）， ferroptosis markers GPX4， and acyl-CoA synthetase long-chain family member 4 （ACSL4） at the mRNA and protein levels.ResultsData analysis identified 10 key genes in the ferroptosis process of NAFLD， including SUMO-specific peptidase 1 （SENP1）， aldo-keto reductase family 1 member C3 （AKR1C3）， and others. Least absolute shrinkage and selection operator- receiver operating characteristic （LASSO-ROC） analysis confirmed that GPX7， LTF， and S100A8 were core genes ［area under the curve（AUC）=0.771–0.821］. KEGG enrichment analysis revealed that these differentially expressed genes were involved in ferroptosis， advanced glycation end-products/receptor （AGE/RAGE）， and other pathways. Correlation analysis of key genes in ferroptosis process of NAFLD showed significant positive correlations between SENP1 and AKR1C3 as well as other genes （P<0.01）， and significant negative correlations between dipeptidyl peptidase 4 （DPP4） and GPX7 as well as other genes （P<0.01）. Immune infiltration analysis showed that myeloid-derived suppressor cells （MDSCs）， activated dendritic cells， and other immune cells were the primary immune cells infiltrating in NAFLD and involved in the ferroptosis process. Differential correlation analysis of immune cell revealed a significant negative correlation between GPX7 and follicular helper T cells as well as others （P<0.01）， while S100A8 showed a significant positive correlation with MDSCs （P<0.01）. In the animal experiments， NAFLD mice with BA intervention showed significantly reduced liver index and lipid droplet deposition. Compared to the normal group， the model group exhibited significantly increased proteins/mRNA levels of S100A8 and ACSL4 （P<0.01） and significantly decreased levels of LTF， GPX7， and GPX4 （P<0.01）. In comparison with the model group， both the silymarin and BA groups partially reversed these trends in a dose-dependent manner.ConclusionBA may inhibit the ferroptosis process and alleviate liver inflammation and lipid deposition by regulating GPX7， LTF， and S100A8. The mechanism is related to the restoration of GPX4 activity and downregulation of ACSL4 expression.关键词：bioinformatics;betulinic acid;molecular docking;non-alcoholic fatty liver disease;ferroptosis30|28|0更新时间：2026-06-30
- 摘要：ObjectiveTo investigate the effects of Celastrus orbiculatus ethylacetate extract （COE） on macrophage polarization and the underlying mechanisms in inhibiting the proliferation and migration of gastric cancer cells.MethodsTHP-1 cells were stimulated with phorbol 12-myristate 13-acetate （PMA）， interleukin-4 （IL-4）， and interleukin-13 （IL-13） to establish an M2 macrophage polarization model. The cells were divided into three groups： M0 group （treated with PMA at 100 μg·L-1）， M2 group （treated with PMA at 100 μg·L-1 + IL-4 and IL-13 at 20 μg·L-1 each）， and M2 + COE group （treated with PMA at 100 μg·L-1 + IL-4 and IL-13 at 20 μg·L-1 each， and COE at 10 g·L-1）. Cell viability was assessed using the CCK-8 assay， and cell proliferation was evaluated by the EdU assay. The mRNA expression levels of macrophage polarization markers， including interleukin-10 （IL-10）， cluster of differentiation 206 （CD206）， tumor necrosis factor-α （TNF-α）， and cluster of differentiation 86 （CD86）， were determined by qRT-PCR. The levels of IL-10 and TNF-α in macrophage supernatants were measured by ELISA. High-content imaging and Western blot were used to assess the effects of conditioned medium from COE-treated macrophages on the migration ability of gastric cancer cells.ResultsCCK-8 and EdU assays showed that， compared with the M2-CM group， the M2 + COE-CM group significantly inhibited the proliferation of gastric cancer cells （P<0.05， P<0.01）. Compared with the M0 group， the mRNA expression levels of IL-10 and CD206 in macrophages were significantly increased in the M2 group （P<0.01）. Compared with the M2 group， the M2 + COE group showed significantly decreased mRNA expression of IL-10 and CD206 （P<0.01）， while the mRNA expression of TNF-α and CD86 was significantly increased （P<0.01）. In addition， the level of IL-10 in the supernatant was decreased， whereas the level of TNF-α was significantly increased （P<0.05， P<0.01）. Western blot analysis demonstrated that， compared with the M2-CM group， the protein expression levels of Vimentin， MMP-2， MMP-9， Snail， and Slug in AGS， HGC-27， and MKN28 cells were significantly reduced in the M2 + COE-CM group （P<0.05， P<0.01）.ConclusionCOE can inhibit the proliferation and migration of gastric cancer cells by regulating macrophage polarization. The underlying mechanisms may be closely associated with the regulation of the epithelial-mesenchymal transition （EMT） process via the TLR4/NF-κB signaling pathway.关键词：Celastrus orbiculatus ethylacetate extract;gastric cancer;proliferation;migration;macrophage polarization36|26|0更新时间：2026-06-30
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Role of Fluid Shear Stress in Pulmonary Fibrosis from Perspective of Lung Linking with All Vessels AI导读
摘要：Pulmonary fibrosis （PF） is a fatal interstitial lung disease characterized by progressive pulmonary scarring and respiratory failure. Current Western medical treatments， such as nintedanib， are limited in their ability to reverse disease progression and are associated with notable adverse effects during long-term use. In traditional Chinese medicine （TCM）， PF is categorized under conditions such as lung atrophy （Fei Wei） and lung impediment （Fei Bi）， with its core pathogenesis attributed to deficiency of healthy Qi， obstruction of collaterals， and cumulative damage that is difficult to restore. In recent years， advances in biomechanical research have increasingly demonstrated that disturbances in fluid shear stress within the pulmonary microenvironment play a critical role in the initiation and progression of fibrosis. According to the TCM theory of lung linking with all vessels， this study systematically elucidates the intrinsic relationship between this classical theory and pulmonary biomechanical regulation from a multidisciplinary perspective. Our analysis suggests that under physiological conditions， appropriate fluid shear stress represents a micro-scale biomechanical manifestation of the lung's role in maintaining the dynamic balance of Qi and blood circulation. In PF， alveolar structural remodeling leads to local flow field disruption， and abnormally elevated or disordered shear stress promotes endothelial-to-mesenchymal transition and aberrant fibroblast activation， thereby accelerating excessive extracellular matrix deposition and disease progression. On this basis， we propose a pathophysiological evolution model characterized by abnormal descending and ascending of lung Qi （Qi）-abnormal mechanical output of lung collaterals （force）-Zang-Fu organ dysfunction. Furthermore， corresponding syndrome differentiation and therapeutic strategies are discussed with consideration to patterns such as Yin deficiency with lung dryness， lung Qi deficiency， lung-kidney Qi deficiency， as well as phlegm-dampness and blood stasis. From the perspective of Qi-collateral-force coupling， this study provides a novel theoretical framework for TCM interventions in PF and offers a reference for the modern biological interpretation and translational research of TCM theories.关键词：pulmonary fibrosis;lung linking with all vessels;fluid shear stress;lung collaterals;biomechanics29|25|0更新时间：2026-06-30 - 摘要：ObjectiveTo investigate the effects of Kummerowia striata extract on inflammatory response， oxidative stress， and gut microbiota in mice with acute liver injury （ALI） induced by carbon tetrachloride （CCl4）.MethodsSixty male Kunming mice were randomly divided into six groups （n=10 per group）： Blank control group， model group， bifendate group （150 mg·kg-1）， and high-， medium-， and low-dose groups of K. striata extract （600， 400， and 200 mg·kg-1， respectively）. All treatments were administered continuously by gavage for 14 days. An ALI model was established by intraperitoneal injection of 0.2% CCl4 in olive oil solution 2 h after the last administration. Serum， liver tissues， and cecal contents were collected 16 h later. Serum levels of alanine aminotransferase （ALT）， aspartate aminotransferase （AST） activity， tumor necrosis factor-α （TNF-α）， and interleukin-6 （IL-6） were measured. The activities of superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px）， as well as the content of malondialdehyde （MDA） were determined in liver tissues. Hepatic histopathological changes were observed by hematoxylin-eosin （HE） staining. Western blot was used to detect the expression levels of phosphorylated nuclear factor-κB p65 （p-NF-κB p65）， phosphorylated extracellular signal-regulated kinase （p-ERK）， phosphorylated c-Jun N-terminal kinase （p-JNK）， phosphorylated p38 mitogen-activated protein kinase （p-p38 MAPK）， nuclear factor erythroid 2-related factor 2 （Nrf2）， heme oxygenase-1 （HO-1）， and Kelch-like ECH-associated protein1 （Keap1） in liver tissues. 16S rDNA high-throughput sequencing technology was used to detect changes in gut microbiota in cecum contents.ResultsK. striata extract significantly reduced serum ALT and AST activities and lowered TNF-α and IL-6 levels in mice with ALI. It also increased SOD and GSH-Px activities， decreased MDA content in liver tissues， and ameliorated histopathological damage. Furthermore， the extract upregulated the protein expression of Nrf2， HO-1， p-NF-κB p65， p-p38 MAPK， p-ERK， and p-JNK， downregulated Keap1 expression， and alleviated gut microbiota dysbiosis.ConclusionK. striata extract exerted a significant protective effect against CCl4-induced acute liver injury in mice. The mechanism may be associated with the activation of Nrf2/HO-1 signaling pathway to alleviate oxidative damage， regulation of nuclear factor-κB （NF-κB）/mitogen-activated protein kinase （MAPK） signaling pathway to suppress inflammatory response， and improvement of gut microbiota dysbiosis via the gut-iver axis.关键词：Kummerowia striata extract;liver injury;nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway;nuclear factor-κB （NF-κB）/mitogen-activated protein kinase （MAPK） signaling pathway;gut microbiota24|6|0更新时间：2026-06-30
- 摘要：ObjectiveTo systematically evaluate the clinical concordance of existing animal models of acute myocardial infarction （AMI） based on the clinical characteristics of AMI in traditional Chinese medicine （TCM） and Western medicine， thus providing suggestions for constructing animal models that conform to the pathological features and TCM syndrome manifestations of AMI.MethodsThe articles related to animal models of AMI were retrieved from domestic and foreign databases such as China National Knowledge Infrastructure （CNKI）， Wanfang Data， and PubMed， with the time interval from January 2010 to January 2026. According to the domestic and international diagnostic criteria and guidelines for AMI and evaluation methods for animal models， this paper summarized， evaluated， and analyzed the clinical characteristics of AMI in TCM and Western medicine. From the pathological mechanisms in Western medicine and the TCM syndrome manifestations， a quantitative evaluation was conducted multiple types of models in terms of the modeling methods， mechanism characteristics， advantages and disadvantages， as well as the degree of concordance with clinical characteristics in both Western and TCM medicine.ResultsExisting animal models of AMI in Western medicine include ischemic， ischemia-reperfusion， chemically induced， cryoablation， hypoxia/reoxygenation， photochemical thrombosis， microembolism， metabolic + surgical， and gene engineering + surgical models. The animal models of AMI in TCM include models with Qi-Yin deficiency syndrome， deficiency-stasis-toxin syndrome， and blood stasis syndrome.ConclusionExisting animal models of AMI show high concordance with core Western medical indicators， but generally lack adequacy in simulating TCM syndrome patterns. They fail to effectively reproduce the holistic manifestation and dynamic evolution process of etiology-pathogenesis-syndrome. Future research should， on the basis of ensuring the stability and reliability of Western medical pathological models， integrate TCM etiological theories to construct a multi-dimensional animal model of AMI combining disease and syndrome. Additionally， an objective and quantified multi-dimensional evaluation system integrating Chinese and Western medicine should be established to promote the in-depth development of integrated Chinese and Western medicine research on AMI.关键词：acute myocardial infarction;animal model;integration of Chinese and Western medicine;syndrome-disease integration;clinical concordance25|5|0更新时间：2026-06-30
- 摘要：Diabetic wound （DW） is one of the serious complications of diabetes and has become a clinical challenge due to its protracted， refractory nature and high recurrence rate. The phosphatidylinositol 3 kinase/protein kinase B （PI3K/Akt） signaling pathway plays a core role in regulating cell proliferation， metabolism， apoptosis， and autophagy， and its functional inhibition is closely associated with impaired DW healing. Modern studies have demonstrated that dysfunction of this pathway can lead to overexpression of inflammatory factors， aggravated oxidative stress， increased apoptosis， and dysregulated autophagy， thereby delaying wound repair. Guided by the holistic concept and treatment based on pattern identification， traditional Chinese medicine （TCM） possesses the advantages of multi-component， multi-target， and holistic regulation. Numerous TCM monomers and compound formulas can regulate the PI3K/Akt signaling pathway， inhibit inflammatory signal transduction mediated by nuclear factor-κB （NF）-κB and others， enhance antioxidant enzyme activities， modulate the balance between apoptosis and autophagy， and promote the expression of vascular endothelial growth factor （VEGF） and other factors， thereby improving cellular functions in a high-glucose microenvironment and synergistically facilitating wound healing. Based on the TCM pathogenesis of "deficiency of vital Qi， stasis and toxin obstructing collaterals"， this paper proposes "reinforcing vital Qi and removing toxin， resolving stasis and dredging collaterals" as the core therapeutic principle for TCM intervention in DW， and summarizes that Chinese medicinals can multi-dimensionally regulate the PI3K/Akt signaling pathway through different treatment methods such as supplementing Qi and activating blood， warming Yang and dredging vessels， and clearing heat and removing toxin， embodying the unique advantage of TCM in "differentiation of disease and pattern， treatment of both the root cause and the manifestations". Future research should integrate systems pharmacology with clinical validation to deeply elucidate the mechanisms of multi-component synergistic regulation of the PI3K/Akt network by Chinese medicinals， providing more sufficient scientific evidence for the prevention and treatment of DW with TCM.关键词：diabetic wounds;phosphatidylinositol 3 kinase/protein kinase B （PI3K/Akt） signaling pathway;traditional Chinese medicine intervention;multi-target therapy21|5|0更新时间：2026-06-30
- 摘要：The rupture of vulnerable atherosclerotic plaques is the major pathological mechanism underlying acute adverse cardiovascular events. Abundant pathological neovascularization within plaques is an important factor contributing to plaque instability. Therefore， inhibiting pathological angiogenesis may represent an effective strategy for stabilizing vulnerable plaques. The theory of collateral disease is an important component of the theoretical system of traditional Chinese medicine （TCM） and provides guidance for the prevention and treatment of microvascular disorders. Based on the theory of collateral disease， this study explored， from a microscopic perspective， the commonalities between collaterals and physiological neovessels in terms of anatomical structure and physiological function， and investigated the similarities in pathological characteristics between diseased collaterals and pathological neovascularization. Taking these similarities as the point of entry， this study integrates TCM theory with modern medicine to interpret the mechanisms by which pathological neovascularization and abnormal hemodynamics contribute to plaque vulnerability， and discusses the scientific connotations of the core pathogenesis of vulnerable atherosclerotic plaques， namely "heart Qi deficiency and collateral obstruction due to blood stasis". Focusing on this core pathogenesis， the therapeutic principle of "dredging and supplementing in the treatment of collateral diseases" is proposed， together with the therapeutic approach of "promoting blood circulation and dredging collaterals while replenishing qi and facilitating collateral flow". In addition， the study investigates the mechanisms by which single Chinese herbs and herbal compound formulas prevent and treat vulnerable atherosclerotic plaques through the multi-target regulation of pathological neovascularization， and analyzes the theoretical convergence between TCM and Western medicine， with the aim of providing new insights into the prevention and treatment of vulnerable atherosclerotic plaques.关键词：atherosclerosis;the theory of collateral disease;dredging and supplementing in the treatment of collateral diseases23|6|0更新时间：2026-06-30
- 摘要：Stable chronic obstructive pulmonary disease （COPD） is a crucial stage for delaying the progression of the disease. Lung and kidney Qi deficiency is the core pathogenesis of stable COPD. The lung-tonifying and kidney-replenishing therapy has remarkable efficacy in treating stable COPD， with distinct characteristics. It can effectively alleviate the clinical symptoms of patients， reduce the frequency and severity of acute exacerbations， improve lung function and immune function， and enhance exercise tolerance and quality of life. In terms of the mechanism of action， numerous studies have shown that the lung-tonifying and kidney-replenishing formulas mainly exert therapeutic effects through regulating immune-inflammatory imbalance， antagonizing oxidative stress， correcting metabolic disorders， restoring protease/antiprotease imbalance， and regulating programmed cell death of alveolar epithelial cells， among other pathways. This paper reviews the ancient medical texts on lung distension and the academic experience of modern physicians to systematically summarize the current application status of the lung-tonifying and kidney-replenishing therapy in the clinical treatment of stable COPD and the biological mechanism it exerts through multiple pathways and multiple targets. However， existing studies often have problems such as short treatment courses， insufficient follow-up， and fragmented mechanism explanations. In the future， large-sample， long-term high-quality evidence-based studies should be conducted， and modern research technologies such as multi-omics， artificial intelligence， and microphysiological systems should be integrated to analyze the core components and action mechanisms of the lung-tonifying and kidney-replenishing formulas in the treatment of COPD through the “component-target-pathway” network. This will provide a high-quality evidence-based basis and innovative strategies for the prevention and treatment of COPD in the era of precision medicine， promoting the inheritance， innovation， and development of traditional Chinese medicine in this field.关键词：chronic obstructive pulmonary disease;lung-tonifying and kidney-replenishing therapy;clinical application;mechanism of action;research progress23|7|0更新时间：2026-06-30
- 摘要：Diabetic kidney disease （DKD） is one of the most common and destructive chronic complications of diabetes. Although conventional therapies can delay disease progression through glycemic control， as well as the inhibition of inflammation， fibrosis， the renin-angiotensin system， and other targets， they are still unable to halt deterioration throughout the entire course of DKD. In recent years， the gut microbiota–microbial metabolite–mitochondrial axis has been proposed as an important framework for understanding the novel pathological mechanisms underlying DKD. By reviewing the relevant literature in China and other countries， this paper found that gut microbiota dysbiosis led to reduced short-chain fatty acids （SCFAs）， disordered bile acids （BAs）， and increased indole derivatives and uremic toxin precursors. These relevant metabolites act on the kidney through the circulation， induce mitochondrial structural and functional damage， and subsequently trigger energy metabolism disorders， oxidative stress， inflammatory responses， and impaired mitophagy， thereby promoting DKD progression. Traditional Chinese medicine may exert synergistic intervening effects by regulating gut microbiota structure， suppressing inflammation and oxidative stress， improving intestinal mucosal barrier function， correcting metabolite abnormalities， and maintaining mitochondrial homeostasis. This paper summarized the characteristics of gut microbiota and metabolic disorders related to DKD， the key links of mitochondrial damage， and their coupled mechanisms. However， current research still mainly focuses on correlational evidence and verification of the causal chain linking metabolites， receptors， and mitochondrial function remains insufficient. Future research should further clarify the specific mechanisms of action by integrating approaches such as gut microbiota depletion and reconstruction， fecal microbiota transplantation， metabolite supplementation， and receptor blockade， providing a reference for the systematic research and clinical translation of traditional Chinese medicine in the prevention and treatment of DKD.关键词：diabetic kidney disease;gut microbiota;gut-kidney axis;microbial metabolite;mitochondrion;traditional Chinese medicine15|4|0更新时间：2026-06-30
- 摘要：Wound healing is a dynamic repair process involving the coordinated participation of multiple cell types， active factors， and signaling networks following tissue injury. In clinical practice， issues such as slow healing progress， persistent non-closure of wounds， and pathological scar formation significantly impair patients' quality of life. Therefore， optimizing healing time and repair quality has become a key focus of clinical research. Current clinical treatments have limitations， including limited efficacy， high cost， high recurrence rates， and excessive pathological scar hyperplasia， highlighting the urgent need for novel intervention strategies. In recent years， with deepening research into the mechanisms of wound healing， the transforming growth factor-β （TGF-β）/Smad signaling pathway， a core pathway regulating fibroblast activation， collagen synthesis， and tissue remodeling， is crucial for maintaining the dynamic balance of wound healing. It can modulate the resolution of inflammation， angiogenesis， and collagen metabolism through stage-specific control of gene transcription， thereby exerting bidirectional regulatory effects during the inflammatory， proliferative， and remodeling phases of wound healing. Traditional Chinese medicine， with its unique advantages of multiple targets， pathways， and mechanisms， can accelerate wound healing and inhibit excessive scar formation by targeting key molecules of the TGF-β/Smad signaling pathway. This article systematically reviewed the mechanisms by which the TGF-β/Smad signaling pathway regulates wound healing， covering four aspects： inflammation and oxidative stress， angiogenesis， apoptosis， and epithelial-mesenchymal transition （EMT）. It also summarized the single herbs， active components of traditional Chinese medicine， herb pairs of traditional Chinese medicine， and formulas that modulate this pathway， aiming to fully exploit the advantages of traditional Chinese medicine in the field of wound healing and provide new ideas for clinical research and new drug development for wound healing.关键词：traditional Chinese medicine;active component;wound healing;transforming growth factor-β （TGF-β）/Smad signaling pathway12|5|0更新时间：2026-06-30
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