Chinese Medicine最新文献

{"title":"Thlaspi arvense attenuates colitis-associated colorectal tumorigenesis through suppression of neutrophil recruitment via the NOD/NF-κB pathway.","authors":"Ziwei Wang, Wenkai Wang, Chaowei Wang, Bijin Dong, Yunchuan Sun, Xinying He, Ling Bi, Yan Wang","doi":"10.1186/s13020-026-01381-5","DOIUrl":"10.1186/s13020-026-01381-5","url":null,"abstract":"<p><strong>Background: </strong>In colitis-associated colorectal cancer (CAC), chronic inflammation is the primary driver of tumorigenesis. A critical event in this process is the massive recruitment of neutrophils, which, while part of the host defense, can paradoxically fuel cancer progression. Excessive neutrophil infiltration contributes to sustained mucosal damage through the release of pro-inflammatory mediators and shapes a tumor-promoting microenvironment. Despite their recognized role, therapeutic strategies specifically targeting pathogenic neutrophil recruitment in CAC are limited. Thlaspi arvense (TA), a traditional medicinal plant, possesses purported anti-inflammatory properties, suggesting its potential utility against CAC. Therefore, this study was designed to evaluate the efficacy of TA in preventing CAC and to delineate its mechanism of action, particularly its impact on neutrophil-driven inflammation.</p><p><strong>Methods: </strong>An azoxymethane/dextran sulfate sodium (AOM/DSS) mouse model of CAC was employed. Mice were administered with TA to evaluate its effects on disease severity, as gauged by body weight change, colon length, tumor burden, and survival rate. Histological and immunofluorescence staining were performed to assess mucosal integrity and the expression of tight junction proteins (ZO-1, Claudin-1). Neutrophil infiltration was quantified by flow cytometry and immunofluorescence. The levels of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IFN-γ) and neutrophil chemoattractants (CXCL1/2) were measured using ELISA and qPCR, respectively. To specifically probe the CXCL1/2-CXCR2 axis, a CXCR2 inhibitor was used as an interventional control. Mechanistic insights were gained through RNA sequencing and Western blot analysis. Furthermore, molecular docking was performed to predict the binding affinity of key TA constituents to core proteins within the NOD/NF-κB pathway.</p><p><strong>Results: </strong>The AOM/DSS mouse model successfully recapitulated the hallmark features of CAC. Treatment with TA, especially at higher doses, markedly attenuated the pathological manifestations, including body weight loss, colon shortening, adenoma formation, and severe inflammatory responses. Consistently, the TA administration restored mucosal integrity and significantly upregulated the expression of tight junction proteins ZO-1 and Claudin-1. At a functional level, TA significantly reduced the production of the neutrophil chemoattractants CXCL1 and CXCL2, which and consequently impaired the interaction with CXCR2 on neutrophils and led to a substantial decrease in neutrophil recruitment. Mechanistic investigation further demonstrated that TA exerted its effects by suppressing the activation of key proteins within the NOD/NF-κB signaling pathway. This suppression resulted in diminished CXCL1/2 expression and a consequent attenuation of the neutrophil-driven pro-tumorigenic microenvironment.</p><p><strong>Conclusions: </strong>We con","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13088638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147715873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Jieduquyuziyin prescription for systemic lupus erythematosus: a system-level therapeutic strategy for immunological recalibration.","authors":"Yihong Gan, Jingqun Liu, Shihui Zhou, Ke Lin, Xinchang Wang, Yongsheng Fan, Li Xu, Jie Bao","doi":"10.1186/s13020-026-01397-x","DOIUrl":"https://doi.org/10.1186/s13020-026-01397-x","url":null,"abstract":"<p><strong>Background: </strong>Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease involving immune dysregulation, metabolic reprogramming, and multi-organ damage. The Jieduquyuziyin prescription (JP), a contemporary Chinese herbal formula based on the Traditional Chinese Medicine principle of \"Jiedu Quyu Ziyin,\" has shown clinical efficacy in SLE. This review aims to synthesize clinical and preclinical evidence explaining how JP achieves systemic therapeutic effects by targeting interconnected pathological pathways in SLE.</p><p><strong>Methods: </strong>We systematically searched PubMed, Web of Science, and CNKI (January 1999-December 2025) for clinical trials, preclinical studies, and multi-omics analyses investigating JP or its bioactive compounds in SLE.</p><p><strong>Results: </strong>Clinical evidence demonstrates that JP-containing regimens significantly reduce SLEDAI scores, alleviate lupus nephritis, lower glucocorticoid requirements, and improve quality of life in SLE patients. Preclinical studies in SLE-prone MRL/lpr mice reveal that JP targets key SLE pathogenic pathways: it restores Th17/Treg balance, suppresses SLE-associated pathogenic B cell proliferation via AKT/mTOR inhibition, and promotes apoptosis of double-negative T cells through UBE2M-mediated Bim upregulation. JP inhibits macrophage IRAK1/ NF-κB signaling, attenuates lupus nephritis by activating renal FXR to suppress TGF-β1/α-SMA-driven fibrosis, and mitigates oxidative damage via Nrf2 activation. Addressing SLE-associated immunometabolic dysfunction, JP reverses pathological glycolytic reprogramming in lymphocytes via AMPK signaling and restores mitochondrial function. Additionally, JP remodels gut microbiota in SLE models, enriching Akkermansia and modulating short-chain fatty acid and bile acid metabolism to reinforce immune homeostasis.</p><p><strong>Conclusion: </strong>This review validates JP as a system-level therapeutic strategy targeting immune dysregulation, metabolic reprogramming, and gut dysbiosis in SLE, supporting the TCM principle of \"Jiedu Quyu Ziyin\" and its integration with modern immunology.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13078005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Schisandrol B protects against lithocholic acid-induced cholestatic liver injury in mice through mitochondrial biogenesis.","authors":"Xiao Yang, Hangfei Liang, Xuan Li, Jianing Tian, Shicheng Fan, Min Huang, Jianbo Wan, Zhong Zuo, Haibiao Guo, Huichang Bi","doi":"10.1186/s13020-026-01342-y","DOIUrl":"10.1186/s13020-026-01342-y","url":null,"abstract":"<p><strong>Background: </strong>Mitochondrial biogenesis plays a vital role in various types of hepatocyte injury. Schisandrol B (SolB), a bioactive lignan isolated from Schisandra sphenanthera, exerts a significant hepatoprotective effect against lithocholic acid (LCA)-induced cholestatic liver injury. Whether mitochondrial biogenesis is involved in the anti-cholestasis effect of SolB remains unknown.</p><p><strong>Methods: </strong>A mouse model of cholestatic liver injury was induced by intraperitoneal injection of LCA. SolB was administered orally twice a day. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bile acids (TBA) and total bilirubin (TBILI), as well as hepatic superoxide dismutase (SOD) activity were measured. Liver pathology was evaluated by toxylin and eosin (H&E) staining. Mitochondrial morphology was examined using electron microscopy. Furthermore, the expression of mitochondrial biogenesis-related genes or proteins was analyzed by RT-qPCR or Western blot.</p><p><strong>Results: </strong>We confirmed that SolB pretreatment (200 mg/kg/d) alleviated LCA-induced liver injury as evidenced by histological and biochemical analyses. SolB alleviated LCA-induced mitochondrial dysfunction in mice, as evidenced by increased mitochondrial DNA (mtDNA) content, superoxide dismutase (SOD) levels, and peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) and mitochondrially encoded cytochrome c oxidase subunit 1 (MTCO1) expression, together with decreased fibroblast growth factor 21 (Fgf21) and growth differentiation factor 15 (Gdf15) gene levels. Transmission electron microscope analysis showed that LCA elicited small, fragmented mitochondria, which were not reversed after SolB pretreatment. However, western blot analysis showed that the expression of mitochondrial dynamics-related proteins, such as dynamin-related protein1 (DRP1), optic atrophy 1 (OPA1), mitofusin 1 (MFN1), and MFN2, was significantly decreased after LCA treatment. Pretreatment with SolB could significantly upregulate DRP1, mitochondrial fission factor (MFF), and fission1 (FIS1) which are crucial to regulate mitochondrial fission. It is worth noting that the protective effect of SolB against LCA-induced liver injury was independent of parkin RBR E3 ubiquitin-protein ligase (PARKIN)-mediated mitophagy as evidenced by decreased PARKIN and microtubule-associated protein light chain 3 (LC3)-II.</p><p><strong>Conclusion: </strong>In summary, this study demonstrated that SolB improved mitochondrial function but had no effect on LCA-induced mitochondrial fragmentation, which provides new insights into better understanding hepatoprotective mechanism of SolB against cholestatic liver injury.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13078053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of Traditional Chinese Medicine in the management of liver disease: targeting gut microbiome.","authors":"Yifan Zhang, Hongkun Li, Fei Yu, Mengmeng Gao, Yang Wang, Siyu Xin, Jiating Yang, Zhiwei Wang, Lujie Xiang, Qingjing Ru, Na Jiang","doi":"10.1186/s13020-026-01395-z","DOIUrl":"https://doi.org/10.1186/s13020-026-01395-z","url":null,"abstract":"<p><p>In recent years, liver disease have become a major contributor to global morbidity and mortality, with current clinical treatments often limited by late diagnosis and rapid progression. This review aims to explore the underexplored role of gut microbiota (GM) in liver disease pathogenesis, and to highlight how Traditional Chinese Medicine (TCM) offers a novel therapeutic approach through indirect modulation of the GM. While conventional pharmacological strategies focus on direct organ-targeting interventions, TCM emphasizes a holistic, multi-target approach that aligns with the complex GM-liver axis. Specifically, we examine the interactions between GM and various liver diseases (alcoholic liver disease, non-alcoholic fatty liver disease, cirrhosis, acute liver injury, autoimmune hepatitis, and hepatocellular carcinoma) and focuses on the indirect axis of \"TCM-GM-liver,\" aiming to elucidate its scientific implications from the perspective of indirect pharmacology. Unlike current research that broadly addresses GM-derived metabolites, this review innovatively details how TCM and natural products regulate specific bacterial phyla and their representative genera to influence disease progression. In conclusion, we emphasize that GM metabolites serve as critical intermediate substances in TCM-mediated hepatoprotection. By elucidating these mechanisms, this review provides a theoretical foundation for developing microbiota-guided therapeutic strategies and advancing novel drug discovery for liver diseases.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13078023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ganoderma lucidum mediates microglial polarization and ameliorates experimental autoimmune encephalomyelitis by reducing oxidative stress and inhibiting NF-κB/STAT3 pathway.","authors":"Lu Zhang, Jie Chen, Sauchu Yuen, Meiling Wu, Wenting Li, Shenyu Yan, Jiangang Shen","doi":"10.1186/s13020-026-01327-x","DOIUrl":"10.1186/s13020-026-01327-x","url":null,"abstract":"<p><p>Multiple Sclerosis (MS) is a neuroinflammatory disease affecting the central nervous system (CNS), for which effective therapeutic strategies remain limited. Ganoderma Lucidum (GL) is a nature healthy food supplement whose effects on MS remain unknown. Using an experimental autoimmune encephalomyelitis (EAE) mouse model, we tested the hypothesis that GL could mitigate MS by inhibiting microglial activation and promoting a shift toward an anti-inflammatory M2-like phenotype. We demonstrate that early preventive administration of GL significantly reduced disease severity, inflammatory infiltration, demyelination, and microglial activation and polarization by promoting M2-like polarization in the spinal cord of EAE mice. Furthermore, using in vitro cellular experiments, GL revealed antioxidant and anti-inflammatory effects by scavenging superoxide (O₂·^-), nitric oxide (NO·) and peroxynitrite (ONOO^-) and down-regulated the expression of IL-1β, TNF-α, IL-6, COX2, and iNOS in the LPS-stimulated microglial cells. GL inhibited the expression of nuclear factor-κB/signal transducer and activator of transcription 3 (NF-κB/STAT3). Taken together, Ganoderma lucidum is a promoting antioxidant and anti-inflammatory healthy supplement to inhibit microglial activation and attenuate the severity and progress of MS pathogenesis by reducing oxidative stress and modulating NF-κB/STAT3 signaling pathways.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Moxibustion delays ovarian aging by regulating mitochondrial biogenesis and improving oocyte quality.","authors":"Yaoli Yin, Yan Xu, Zemin Li, Meilin Chen, Ziwei Song, Hongxiao Li, Ge Lu, Meihong Shen","doi":"10.1186/s13020-026-01375-3","DOIUrl":"10.1186/s13020-026-01375-3","url":null,"abstract":"<p><strong>Background: </strong>The growing trend of delayed childbearing in contemporary society has made fertility preservation a significant issue, prompting the search for diverse therapeutic options. Conversely, moxibustion is gaining increasing attention as a potential non-pharmacological therapy for supporting reproductive health.</p><p><strong>Methods: </strong>Mice aged 2 to 14 months were assessed for ovarian function detection to determine the age of reproductive senescence and to identify the optimal time for moxibustion intervention to delay senescence. Oocyte quality and mitochondrial function assessments were conducted to investigate the role of mitochondrial biogenesis in ovarian aging and the underlying mechanisms following moxibustion intervention.</p><p><strong>Results: </strong>Mice aged 10 months demonstrated ovarian dysfunction associated with aging. Moxibustion significantly elevated hormone levels, increased the number of growing follicles, enhanced embryo implantation and viable birth rates, and reduced embryonic mortality in aging mice. The most pronounced effects were observed in 10-month-old mice. These beneficial outcomes might be linked to improved oocyte quality. Crucially, moxibustion positively increased mitochondrial quantity, enhanced mitochondrial quality, and influenced mitochondrial biogenesis, an effect comparable to that of the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) agonist valproic acid. Furthermore, the beneficial effects of moxibustion were partially attenuated by a PGC-1α inhibitor.</p><p><strong>Conclusions: </strong>Moxibustion, as a non-pharmacological intervention, may mitigate ovarian aging and serve as an effective therapeutic strategy for extending human fertility.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZhiXiaoSanZheng formula ameliorates podocyte injury in diabetic kidney disease by inhibiting ferroptosis: integrated network pharmacology and experimental validation.","authors":"Shaofeng Zhou, Huijuan Zheng, Xinghua Zhang, Chenhui Xia, Weimin Jiang, Yaotan Li, Jiale Zhang, Shiwei Ruan, Binhua Ye, Weiwei Sun, Yaoxian Wang","doi":"10.1186/s13020-026-01389-x","DOIUrl":"10.1186/s13020-026-01389-x","url":null,"abstract":"<p><strong>Background: </strong>Diabetic kidney disease (DKD) is widely recognized as a major contributor to end-stage renal disease, in which podocyte injury serves as an important pathological basis for disease progression. ZhiXiaoSanZheng Formula (ZXSZF), an empirically derived traditional Chinese medicine prescription, has shown therapeutic potential in DKD; however, its molecular mechanisms remain unclear. This study investigated whether ZXSZF protects podocytes by modulating ferroptosis-related pathways.</p><p><strong>Methods: </strong>The chemical profile of ZXSZF was analyzed by LC-MS/MS. Potential bioactive compounds were screened through SwissADME, and putative targets were predicted using SwissTargetPrediction. Overlapping targets among ZXSZF, DKD, and ferroptosis were identified and analyzed through protein-protein interaction and functional enrichment analyses. The predicted mechanisms were further validated in a unilateral nephrectomy plus STZ-induced DKD rat model and in AGEs-stimulated MPC5 podocytes.</p><p><strong>Results: </strong>LC-MS/MS analysis identified 94 chemical constituents in ZXSZF. Network pharmacology analysis suggested that antioxidant and ferroptosis-related pathways centered on NRF2 may represent potential regulatory nodes of ZXSZF. In DKD rats, ZXSZF reduced albuminuria and improved renal histopathological changes, accompanied by restoration of podocyte markers and attenuation of ferroptosis-associated alterations. In AGEs-stimulated podocytes, ZXSZF decreased lipid peroxidation and iron accumulation while enhancing cellular antioxidant capacity. These effects were associated with increased NRF2 signaling and upregulation of SLC7A11 and GPX4. Pharmacological inhibition of NRF2 with ML385 partially attenuated the protective effects of ZXSZF.</p><p><strong>Conclusions: </strong>ZXSZF alleviates podocyte injury in DKD and its renoprotective effects are associated with modulation of ferroptosis-related processes involving the NRF2/SLC7A11/GPX4 pathway. The present study provides experimental evidence for the mechanistic basis of ZXSZF and supports its potential role as a complementary therapeutic option in DKD management.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13054979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Si-Ni-San alleviates depression-like behavior via regulating the gut microbiota-tryptophan metabolism-AhR/NF-κB pathway axis.","authors":"Qiang Xiao, Zhaoyi Wen, Huang Zhan, Han Zhao, Yukun Jiao, Dehua Huang, Hui Li, Congcong Chen","doi":"10.1186/s13020-026-01390-4","DOIUrl":"10.1186/s13020-026-01390-4","url":null,"abstract":"<p><strong>Background: </strong>Si-Ni-San (SNS), a classic herbal formula from the Treatise on Cold Damage Diseases, is used to treat depression by relieving \"liver qi stagnation\". However, the underlying mechanism remains unclear.</p><p><strong>Purpose of the research: </strong>This study aimed to investigate the mechanism by which SNS alleviates depression-like behavior, specifically focusing on its role in modulating gut microbiota and host tryptophan metabolism.</p><p><strong>Methods: </strong>A depression model was induced in mice by chronic unpredictable mild stress (CUMS). The antidepressant effects of SNS were evaluated through behavioral tests. Integrated untargeted and targeted metabolomics, alongside 16S rRNA sequencing, were utilized to identify potential gut-brain signaling molecules. Molecular interactions between the gut-brain signaling molecule and its target were validated by surface plasmon resonance (SPR) and molecular docking. Key protein expression was measured via Western blot and ELISA. Finally, the function of gut microbiome-derived indole-3-acetic acid (IAA) as a key gut-brain signaling molecule was confirmed by oral supplementation experiments.</p><p><strong>Results: </strong>SNS significantly alleviated CUMS-induced depression-like behaviors. Multi-omics analysis revealed that SNS reversed tryptophan metabolic disorders and elevated gut microbiome-derived IAA levels in both the colon and prefrontal cortex, which was attributed to the enrichment of Lactobacillus. Further investigations confirmed that IAA directly binds to and activates the aryl hydrocarbon receptor (AhR), thereby inhibiting NF-κB pathway-mediated neuroinflammation. Moreover, oral supplementation with IAA replicated the antidepressant effects of SNS and suppressed CUMS-induced neuroinflammation via the AhR/NF-κB signaling pathway.</p><p><strong>Conclusion: </strong>SNS alleviates depression-like behavior by modulating gut microbiota-mediated tryptophan metabolism to enhance IAA production, thereby activating central AhR signaling and suppressing NF-κB-mediated neuroinflammation.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13054972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erianin facilitates pyroptosis in endometrial cancer via targeting m6A reader YTHDF1.","authors":"Wan Shu, Xing Zhou, Rong Zhao, Kejun Dong, Xiaoyu Shen, Guanxiao Chen, Shuangshuang Cheng, Qi Zhang, Ting Zhou, Jiarui Zhang, Tangansu Zhang, Shuyang Yu, Haojia Li, Yuwei Yao, Yan Liu, Jun Zhang, Hongbo Wang","doi":"10.1186/s13020-025-01313-9","DOIUrl":"10.1186/s13020-025-01313-9","url":null,"abstract":"<p><strong>Background: </strong>Endometrial cancer (EC) is a gynecological malignancy that originates from the endometrial epithelium and has a poor prognosis when advanced, recurrent, or metastatic. The limited therapeutic efficacy and severe adverse effects of conventional chemotherapy in advanced EC highlight the urgent need to develop more effective therapeutic drugs. Accumulating clinical evidence has revealed that natural compounds possess pharmacological advantages, including low toxicity and multi-target mechanisms. Erianin is a natural, small-molecule compound isolated from Dendrobium chrysotoxum Lindl that has multiple pharmacological effects. However, the effects of erianin on EC have not been confirmed and its anticancer mechanisms remain unclear.</p><p><strong>Methods: </strong>Erianin was identified as a potent natural compound against EC through compound library screening. CCK-8 assays, colony formation assays, Edu experiments, and Live/Dead cell staining assays were used to analyze the anti-proliferative activity of erianin. Morphological characteristics, transmission electron microscopy, lactate dehydrogenase release assays, and western blot assays were used to evaluate the activation of pyroptosis. A transcriptome sequencing analysis was conducted to identify the potential mechanism of erianin. Biotin-erianin was synthesized and 20-k human proteome microarray was used to identify its direct targets. Molecular docking and cellular thermal shift assays (CETSA) were used to investigate whether erianin would bind to YTH domain family proteins (YTHDF1). To evaluate the in vivo therapeutic potential of erianin, an EC xenograft model was established and mechanistic investigations incorporating hematoxylin and eosin and immunohistochemical (IHC) staining, and western blot assays were conducted.</p><p><strong>Results: </strong>Erianin inhibited the cell proliferation of EC cells and promoted pyroptosis through the caspase-3/gasdermin E (GSDME) pathway. Mechanistically, a crucial role for FOXM1/RRM2-mediated DNA damage in erianin-induced pyroptosis was established. Protein microarrays indicated that erianin-biotin directly targeted the m6A reader, YTHDF1. Erianin was confirmed to bind to YTHDF1 using molecular docking and CETSA. Molecular studies indicated that erianin inhibited YTHDF1, recognized m6A-modified FOXM1, and promoted FOXM1 mRNA degradation, which led to DNA damage and caspase-3-mediated GSDME cleavage. Erianin also substantially inhibited EC tumor growth in EC models.</p><p><strong>Conclusion: </strong>Erianin directly targeted YTHDF1 to suppress the FOXM1/RRM2 axis and consequently promoted caspase-3/GSDME-dependent pyroptosis in EC cells. Our findings provide a new strategy for further clinical exploration of EC.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13054981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture inhibited neuronal apoptosis through PGAM5/FUNDC1-dependent mitophagy after ischemic stroke.","authors":"Li Zhou, Yicheng Peng, Mingchao Fu, Mei Zhou, Chengcai Zhang, Xichen Yang, Yongdan Cun, Simei Zhang, Na Chen, Rong Ning, Yaju Jin, Zuhong Wang, Hong Xin, Pengyue Zhang","doi":"10.1186/s13020-026-01383-3","DOIUrl":"10.1186/s13020-026-01383-3","url":null,"abstract":"<p><p>Neuronal apoptosis persists throughout ischemic stroke. This leads to massive neuron loss and severely impairs recovery of neurological function. Clinical evidence has confirmed that electroacupuncture (EA) effectively improves neurological function after ischemic stroke; however, the underlying mechanism remains to be fully elucidated. In this study, we found that apoptosis and autophagy were activated after ischemic stroke. EA further upregulated autophagy and inhibited neuronal apoptosis in the ischemic stroke model. Furthermore, EA's neuroprotective effect was linked to mitophagy activation by upregulating PGAM5 expression, which promoted FUNDC1 dephosphorylation and enhanced the interaction between FUNDC1 and LC3, ultimately activating PGAM5/FUNDC1-dependent mitophagy. Enhanced mitochondrial autophagy reduced ROS production and Cyt c release from damaged mitochondria, thereby inhibiting Caspase3 activation and subsequent neuronal apoptosis. Meanwhile, EA also upregulated the level of FUNDC1 and further promoted mitophagy through the PGAM5/FUNDC1 pathway. Notably, lateral ventricle injection of 3-MA inhibited mitophagy and significantly reversed the neuroprotective effect of EA. In summary, the neuroprotective effect of EA against ischemic stroke might be achieved by inhibiting neuronal apoptosis through PGAM5/FUNDC1-dependent mitophagy.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13047806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147615975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}