Chinese Medicine最新文献

{"title":"Remote electroacupuncture conditioning protects the heart via fine-tuning the dual role of the SDF-1α/CXCR4 axis in myocardial ischemia-reperfusion injury.","authors":"Senlei Xu, Jianfeng Lian, Shiyu Chen, Yan Zuo, Hui Xiong, Ying Lin, Yihuang Gu, Hongru Zhang","doi":"10.1186/s13020-026-01470-5","DOIUrl":"https://doi.org/10.1186/s13020-026-01470-5","url":null,"abstract":"<p><strong>Background: </strong>Remote electroacupuncture (EA) conditioning on forearm protects against myocardial ischemia-reperfusion injury (MIRI). However, the cardioprotective mechanisms of RIC have not been fully elucidated. This study aimed to investigate whether EA could balance the pro-survival and pro-inflammatory responses in MIRI rats via SDF-1α/CXCR4 axis.</p><p><strong>Methods: </strong>SD rats were subjected to MIRI and underwent EA treatment before reperfusion therapy. Infarct size, cardiac function, and neutrophil infiltration were evaluated after 24-h of reperfusion. The mRNA and protein levels of SDF-1α in the myocardial border and infarct zones, were measured by RT-qPCR and Western blotting to reveal its spatial distribution. We examined serum SDF-1α levels and its myocardial scavenger receptor CXCR7 expression to elucidate the mechanism underlying its spatial distribution. Then, CXCR4/ERK pathway was evaluated at 15 min and 24 h after EA to examine the time-dependent dual effects of SDF-1α on CXCR4.</p><p><strong>Results: </strong>Our results showed that EA attenuated infarct size and mortality, improved cardiac function after 24 h of MIRI. We identify that SDF-1α is a key humoral factor mediating EA-induced cardioprotection. In ischemic myocardium, the infarct zone exhibited a higher SDF-1α concentration than the border zone following EA treatment, a difference potentially linked to the elevated expression of CXCR7 in the border zone. In the early phase of reperfusion (15 min), our study showed that EA promoted the expression of the CXCR4 receptor, which in turn triggered ERK activation. This rapid ERK activation via SDF-1α/CXCR4 promoted cardiomyocyte survival and attenuated reperfusion-induced apoptosis. While at 24 h post-reperfusion, saturating signals of SDF-1α by EA downregulated CXCR4 expression, along with phosphorylation of its downstream effectors ERK and NF-κB p65. This coordinated downregulation facilitates inflammatory resolution by promoting neutrophil apoptosis.</p><p><strong>Conclusions: </strong>Cardioprotection by EA can be mediated by humoral factors SDF-1α that accumulate in infarct myocardium. SDF-1α triggers pro-survival CXCR4/ERK signaling at 15 min of reperfusion, whereas it promotes neutrophil apoptosis via CXCR4 degradation to facilitate inflammatory resolution by 24 h, thereby fine-tuning the dual role of the SDF-1α/CXCR4 axis in MIRI.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13483163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788866","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":"Acupuncture regulates mitochondrial homeostasis in traumatic brain injury: current evidence, mechanistic hypotheses, and translational challenges.","authors":"Guanglei Li, Luxi Cao, Sisi Zhao, Yingyu Fang, Zhentao Peng, Feidan Deng, Peng Qing, Mingmin Zhu, Yimin Zhang, Shujun Lin","doi":"10.1186/s13020-026-01481-2","DOIUrl":"https://doi.org/10.1186/s13020-026-01481-2","url":null,"abstract":"<p><strong>Background: </strong>Traumatic brain injury (TBI) is associated with high morbidity, disability, and long-term neurological sequelae. Mitochondrial dysfunction is a central component of secondary injury after TBI, contributing to impaired energy metabolism, oxidative stress, calcium dysregulation, neuroinflammation, and neuronal apoptosis.</p><p><strong>Main body: </strong>This review summarizes current evidence regarding acupuncture-mediated regulation of mitochondrial homeostasis after TBI, focusing on structural homeostasis, quantitative homeostasis, and functional/metabolic homeostasis. We distinguish direct evidence from TBI models, indirect evidence from related brain injury models, and hypothesis-generating mechanisms. Particular attention is given to mitochondrial dynamics, mitochondrial biogenesis, mitophagy, energy metabolism, oxidative stress, calcium signaling, mitochondrial membrane potential, apoptosis, intercellular mitochondrial transfer, and putative upstream neural and humoral pathways.</p><p><strong>Conclusion: </strong>Current preclinical evidence suggests that acupuncture, particularly electroacupuncture, may influence mitochondrial homeostasis after TBI through multidimensional and context-dependent mechanisms. However, direct TBI-specific evidence remains limited, and several proposed mechanisms require further validation before acupuncture-mediated mitochondrial regulation can be considered a clinically established therapeutic strategy.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13474900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757954","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":"Advances in Chinese herbal medicine for diabetic wound treatment: from tradition to innovation.","authors":"Zhiqun Hong, Xinyi Liu, Bo Liu, Ye Hu, Huaqiong Li, Zhiqiang Yan, Bo Li","doi":"10.1186/s13020-026-01480-3","DOIUrl":"10.1186/s13020-026-01480-3","url":null,"abstract":"<p><p>Diabetic wounds represent one of the most intractable complications of diabetes, arising from a highly complex and self-perpetuating pathological microenvironment. This milieu is characterized by chronic inflammation, oxidative stress, impaired angiogenesis, peripheral neuropathy, immune dysregulation, recurrent infection, and marked dysfunction of resident cells and the extracellular matrix (ECM). These intertwined abnormalities not only hinder wound closure but also significantly increase the risk of chronic infection, amputation, and disability, thereby imposing substantial clinical and socioeconomic burdens. Conventional therapies, which typically target isolated aspects of wound pathology, often fail to disrupt the vicious cycle of non-healing, underscoring the urgent need for integrated, multi-target therapeutic strategies. Chinese herbal medicine (CHM) encapsulates a holistic therapeutic paradigm that is intrinsically aligned with the multi-factorial nature of diabetic wound management. CHM offers a diverse array of bioactive ingredients, including polysaccharides, saponins, flavonoids, alkaloids, and phenolics, that collectively exert anti-inflammatory, antioxidant, pro-angiogenic, neuroprotective, immunomodulatory, antimicrobial, and pro-proliferative effects. Moreover, many of these ingredients exhibit pleiotropic effects, enabling concomitant modulation of multiple pathological pathways to address the inherent complexity of diabetic wounds. However, the clinical translation of raw CHM is frequently hindered by poor bioavailability and rapid degradation at the wound site. Recent advances in CHM-based innovative delivery platforms have provided a transformative framework to overcome these limitations. This review highlights the emergence of CHM-loaded hydrogels and CHM-derived plant exosome-like nanovesicles (PELNs) as next-generation interventions. CHM-loaded hydrogels act as biomimetic scaffolds that facilitate controlled release and adaptively respond to microenvironmental cues (e.g., pH and reactive oxygen species (ROS)). Simultaneously, CHM-derived exosome-like nanovesicles serve as natural, biocompatible nanocarriers that enhance cellular uptake and molecular signaling, promoting regenerative healing through intercellular communication pathways. In this review, we systematically summarize the pathological features of diabetic wounds and synthesize the modern pharmacological mechanisms of representative CHM ingredients. We further evaluate the synergistic integration of CHM with advanced biomaterials and nanotechnology, emphasizing their translational potential from preclinical models to clinical evidence. By bridging traditional wisdom with cutting-edge bioengineering, these platforms offer a robust evidence-based framework for the modernized management of diabetic wounds.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13436137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148672952","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":"Yiqi Huoxue Jiedu formula protects against sepsis-associated lung injury by modulating macrophage mitophagy and mtDNA-STING signaling.","authors":"Shuqi Ma, Qiusha Pan, Jingnan Lin, Ruifeng Zeng, Xiaotu Xi, Ye Ye, Zhuoxu Gu, Kaiqiang Zhong, Suyi Yang, Lin Wang, Jun Li, Rui Chen","doi":"10.1186/s13020-026-01475-0","DOIUrl":"10.1186/s13020-026-01475-0","url":null,"abstract":"<p><strong>Background: </strong>Yiqi Huoxue Jiedu Formula (YHJF) is a traditional Chinese medicine formula that has been used as an adjunctive therapy for sepsis for nearly two decades. Previous clinical studies showed that YHJF improves Sequential Organ Failure Assessment (SOFA) scores and modulates gut microbiota in elderly patients with pneumonia-associated sepsis. However, the mechanism by which YHJF protects against sepsis-associated acute lung injury (SALI) remains unclear.</p><p><strong>Methods: </strong>A murine SALI model was established by cecal ligation and puncture (CLP). Therapeutic effects were evaluated by histopathology, micro-CT, pulmonary function assessment, and ELISA. Mechanistic studies included proteomic analysis of lung tissues and LPS-stimulated MH-S macrophages, pharmacological modulation with Mdivi-1 and urolithin A (UA), macrophage-epithelial co-culture, HPLC fingerprinting, UPLC-HRMS, and molecular docking.</p><p><strong>Results: </strong>YHJF significantly improved 7-day survival and ameliorated lung injury, pulmonary edema, respiratory dysfunction, and systemic inflammation in mice with CLP-induced SALI. Proteomic profiling and subsequent functional assays suggested that enhanced mitophagy in macrophages represents a central protective mechanism. In vivo, YHJF increased autophagosome formation and PINK1/Parkin co-localization in BALF-derived alveolar macrophages. In vitro, YHJF restored mitochondrial homeostasis by activating PINK1/Parkin-dependent mitophagy in macrophages. This was accompanied by reduced cytoplasmic mtDNA leakage, downregulated cGAS expression, and suppression of the STING-TBK1-IRF3 pathway and subsequent type I interferon responses. Pharmacological inhibition of mitophagy with Mdivi-1 abolished these protective effects of YHJF, whereas activation with UA augmented them, demonstrating that mitophagy is necessary for YHJF-mediated protection. In a macrophage-epithelial co-culture system, YHJF-treated macrophages alleviated LPS-induced apoptosis in MLE-12 alveolar epithelial cells. Furthermore, chemical analysis integrated with molecular docking identified aloe-emodin, rhein, and genistein as candidate bioactive constituents of YHJF that likely contribute to its regulation of macrophage mitophagy.</p><p><strong>Conclusion: </strong>YHJF protects against SALI by restoring macrophage mitophagy and suppressing mtDNA-STING-mediated inflammatory signalling. These findings support YHJF as a potential therapeutic strategy for sepsis-associated lung injury.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435792/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148672927","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":"Self-assembled structures as a material basis for indirect pharmacology in Traditional Chinese Medicine.","authors":"Jian Li, Wei Zhang, Jiayu Ye, Hualin Peng","doi":"10.1186/s13020-026-01471-4","DOIUrl":"10.1186/s13020-026-01471-4","url":null,"abstract":"<p><p>Indirect pharmacology is increasingly invoked to explain how Traditional Chinese Medicine (TCM) and natural products produce therapeutic effects through inter-organ communication and distributed physiological regulation rather than through direct action on a single molecular target. In this context, most mechanistic discussions emphasize downstream mediators, including microbial metabolites, immune signals, and endocrine factors, but pay less attention to the material form in which complex preparations are administered. This review examines the possibility that self-assembled structures in decoctions constitute an underappreciated upstream determinant of indirect pharmacology. Decoctions are not simply molecular solutions; during preparation and after exposure to biological environments, they can form colloids, aggregates, and multicomponent co-assemblies. These material states may influence intestinal localization, mucosal retention, microbial access, barrier interactions, and the spatial pattern of mediator generation. We synthesize evidence from two related lines of research: naturally occurring aggregates in traditional decoctions and bottom-up assemblies constructed from isolated phytochemicals. Across representative case studies, current evidence supports a role for supramolecular organization in shaping exposure and interface-level behavior, but direct causal links to defined mediator chains and distal organ outcomes remain limited. We therefore outline methodological strategies for testing structure-interface-mediator relationships more rigorously in future studies.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13421750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148629446","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":"Forsythoside A alleviates experimental autoimmune encephalomyelitis by targeting Tnfaip2.","authors":"Ping Tang, Guibao Luo, Huihui Xue, Chunsheng Yang","doi":"10.1186/s13020-026-01476-z","DOIUrl":"10.1186/s13020-026-01476-z","url":null,"abstract":"<p><strong>Background: </strong>Multiple sclerosis (MS) is a debilitating neuroinflammatory disease. Experimental autoimmune encephalomyelitis (EAE) is a commonly used rodent model for MS. Forsythoside A (FA), a natural compound derived from Forsythia suspensa, exhibits anti-inflammatory and neuroprotective properties; however, its efficacy in EAE and its underlying mechanism remain unclear.</p><p><strong>Purpose: </strong>To explore the therapeutic effect of FA on EAE and its mechanism.</p><p><strong>Methods: </strong>EAE was induced in C57BL/6 mice treated with FA (20/60 mg/kg) from day 7. Clinical scores, histopathology (H&E, LFB, immunofluorescence), flow cytometry, and spinal cord RNA sequencing were analyzed. Network pharmacology, molecular docking, molecular dynamics (MD) simulations, and surface plasmon resonance (SPR) were employed to identify and validate the target of FA. In vitro studies using BV2 microglia with Tnfaip2 knockdown/overexpression confirmed the mechanism via qRT-PCR and Western blot.</p><p><strong>Results: </strong>FA treatment dose-dependently alleviated clinical severity. While the 20 mg/kg dose showed a trend toward improvement without statistical significance, the 60 mg/kg dose significantly reduced CNS inflammation and demyelination. FA decreased peripheral Th1 cells in EAE mice. It suppressed microglial activation and pro-inflammatory markers (IL-1β, TNF-α, iNOS) expression. Transcriptomics and network analysis pinpointed TNF-α-induced protein 2 (Tnfaip2) in the TNF pathway. FA directly bound Tnfaip2 (K_D = 28 µM), validated by docking, MD simulations, and SPR. In vitro, FA inhibited LPS-induced pro-inflammatory polarization and the Tnfaip2/NF-κB pathway in BV2 cells. Tnfaip2 overexpression abolished the anti-inflammatory effects of FA.</p><p><strong>Conclusion: </strong>FA ameliorates EAE by suppressing pro-inflammatory microglial polarization via directly targeting Tnfaip2 and inhibiting the NF-κB pathway. This identifies the Tnfaip2/NF-κB axis as a potential therapeutic target for MS.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13418143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618696","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":"Macrophage membrane-functionalized biomimetic Yiqi Huoxue formula nanoparticles improve atherosclerosis by regulating smooth muscle cell phenotypic transition via the KLF4/NF-κB pathway.","authors":"Yanqing Li, Hongyuan Wang, Yi Guan, Jinli Zhuang, Xiaohong Yang, Yanting Chen, Shengyu Cun, Jianfeng Li, Ya Qin, Quan Xie","doi":"10.1186/s13020-026-01477-y","DOIUrl":"10.1186/s13020-026-01477-y","url":null,"abstract":"<p><p>This study aimed to analyze the active ingredients of the compound preparation of Yiqi Huoxue (YQHX) and evaluate the therapeutic effect of its nanoparticles (MM/YQHXF-NPs) on atherosclerosis (AS). First, the active ingredient in the YQHX formulation was identified by LC-MS analysis. Subsequently, transmission electron microscopy (TEM) tests particle size. Mapping tests nanoparticle surface elements. Dynamic light scattering (DLS) tests nanoparticle size and distribution. ZETA tests nanoparticle surface potential. HPLC tests drug release. The results showed that these nanoparticles were spherical, approximately 100 nm in size, and had good dispersion. The P element content of MM/YQHXF-NPs increased after cell membrane coating, and their hydrodynamic size also increased accordingly, but the Polymer dispersity index (PDI) value was low, indicating good monodispersity. In addition, the nanoparticle surface had a weak negative charge, the encapsulation efficiency of YQHXF was 59.4%, and the drug loading rate was 5.61%. In cell-based experiments, MM/YQHXF-NPs showed no cytotoxicity towards A7r5 cells at a concentration of 150 μg/mL. The study found that ox-LDL-induced A7r5 cell-to-foam cell transformation was significantly inhibited. Oil Red O staining revealed that MM/YQHXF-NPs reduced lipid accumulation. In addition, YQHXF and its active component, salvianolic acid B, can inhibit the foam cell formation of A7r5 cells. Furthermore, MM/YQHXF-NPs modulated the phenotype of smooth muscle cells, inhibiting the expression of genes such as Myh9, Icam-1, Vcam-1, Tnfrsf11b, Cd68, Lgals3, and Abca1, while promoting the expression of Myh11 and Smtn. Mechanistic studies revealed that MM/YQHXF-NPs exerted their effects by inhibiting the Krüppel-like factor 4 (KLF4) and NF-κB signaling pathways. In a high-fat diet, ApoE^-/- mice model of AS, MM/YQHXF-NPs demonstrated significant therapeutic efficacy. H&E and Oil Red O staining revealed that MM/YQHXF-NPs mitigated pathological changes, reduced plaque size, and lowered serum TC, TG, LDL, and HDL levels. They also stabilized atherosclerotic plaques by increasing fiber area and promoting SM22α and SM-MHC expression. Consistent with the results from cell-based experiments, MM/YQHXF-NPs effectively inhibited the transformation of arterial smooth muscle cells (SMCs) into foam cells in vivo and suppressed the activation of KLF4 and NF-κB signaling pathways. In summary, MM/YQHXF-NPs can effectively prevent the transformation of SMCs into foam cells by inhibiting the KLF4 and NF-κB signaling pathways, thereby alleviating AS. These results provide a theoretical basis for MM/YQHXF-NPs as a potential therapeutic drug for AS.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13404646/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599684","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":"Yiyi Fuzi Baijiang formula protects against DSS-induced colitis by orchestrating the gut barrier-microbiota-metabolism axis.","authors":"Yin Bao, Qiang Ao, Meng Wang, Xiaoling Mao, Jun Zhu, Mingyue Zhang, Yang Chen, Hong Zhu, Jun Gao","doi":"10.1186/s13020-026-01478-x","DOIUrl":"10.1186/s13020-026-01478-x","url":null,"abstract":"<p><strong>Background: </strong>Inflammatory bowel disease (IBD) is a relapsing inflammatory disorder of the gastrointestinal tract with increasing global incidence. Current therapies are often limited by side effects, loss of efficacy, and high cost, underscoring the need for safer and more effective alternatives, particularly multi-target agents derived from natural products.</p><p><strong>Purpose: </strong>This study aimed to elucidate the protective mechanisms of Yiyi Fuzi Baijiang formula (YFB), a traditional Chinese medicine (TCM) formulation, against dextran sulfate sodium (DSS)-induced acute colitis, focusing on its systemic regulation of the gut barrier-microbiota-metabolism axis.</p><p><strong>Methods: </strong>We employed an integrated approach combining network pharmacology, UPLC-Q-TOF-MS/MS-based phytochemical analysis, in vivo evaluation in a DSS-induced colitis mouse model, 16S rRNA gene sequencing, and untargeted metabolomics to assess the effects of YFB and uncover its mechanisms of action.</p><p><strong>Results: </strong>Network pharmacology predicted, and experiments confirmed, that core YFB components (e.g., quercetin, kaempferol) act via IL-17, TNF, and NF-κB pathways. YFB administration dose-dependently improved disease activity index, colon shortening, and histopathology in colitis mice. It restored intestinal barrier integrity by upregulating ZO-1, Occludin, and MUC2, while suppressing pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-17A) and NF-κB activation. Critically, YFB promoted epithelial repair by restoring the expression of intestinal stem cell marker LGR5 and progenitor cell marker SOX9, and by normalizing the aberrant increase in endocrine cell marker CHGA. YFB treatment was associated with reversal of DSS-induced gut microbiota dysbiosis, restoration of diversity, enrichment of beneficial bacteria (e.g., Lachnospiraceae), and suppression of opportunistic pathogens (e.g., Enterobacteriaceae). Untargeted metabolomics showed that YFB treatment was associated with modulation of DSS-altered fecal metabolites (e.g., fatty acids, bile acids) and pathways such as \"microbial metabolism in diverse environments\".</p><p><strong>Conclusion: </strong>YFB, when administered concomitantly with DSS, protects against DSS-induced colitis via the synergistic effects of its multi-component system. Its mechanism entails systemic regulation of the gut barrier-microbiota-metabolism axis, involving suppression of NF-κB-driven inflammation, promotion of intestinal epithelial repair (via LGR5/SOX9/CHGA modulation), restoration of the intestinal barrier, alterations in gut microbiota, and modulation of host-microbial co-metabolism. These findings provide a scientific basis for YFB's clinical application and highlight the value of TCM formulations in managing complex multi-factorial diseases.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13393498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148560989","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":"Medicine-food homologous bioactives in metabolic dysregulation-associated osteoporosis: a review of preclinical evidence and potential liver-bone and gut-bone actions.","authors":"Wen Fan, Beilei Shi, Ze Gao, Yan Cui, Xiaofeng Zhu","doi":"10.1186/s13020-026-01453-6","DOIUrl":"10.1186/s13020-026-01453-6","url":null,"abstract":"<p><strong>Background: </strong>Osteoporosis is increasingly linked to metabolic dysregulation. Medicine-food homologous (MFH) materials contain diverse natural bioactives with reported osteoprotective effects, but their overall evidence landscape remains insufficiently integrated.</p><p><strong>Purpose: </strong>To synthesize preclinical evidence on MFH-derived bioactives that improve osteoporosis-related phenotypes and to discuss their possible trans-organ actions under metabolic disturbance.</p><p><strong>Methods: </strong>PubMed, Web of Science, Scopus, and CNKI were searched from January 2000 to September 2025. Original in vivo or in vitro studies were included when a defined MFH-derived constituent or standardized single-material extract was tested in an osteoporosis-relevant model and reported both bone-related and metabolism-related outcomes.</p><p><strong>Results: </strong>A total of 38 bioactive components from 24 MFH materials were identified and regrouped into seven higher-level natural-product categories, including flavonoids, phenolic and polyphenolic compounds, polysaccharides, saponins, terpenoids, proteins/peptides, and other specialized metabolites. Across studies, osteoprotective effects were frequently accompanied by parallel improvements in lipid metabolism, inflammatory status, oxidative stress, gut microbiota, or related metabolites. These findings suggest that MFH bioactives may act beyond bone-local signaling alone. In the discussion, this pattern was further interpreted through liver-bone and gut-bone.</p><p><strong>Conclusion: </strong>MFH-derived bioactives show potential to improve osteoporosis-related phenotypes and may exert broader systemic regulatory effects, although specific mediators and causal links still require validation.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390145/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561028","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":"Single-cell transcriptomics reveals how Shenfu Qiangxin pill ameliorates HFpEF by modulating cardiac cellular heterogeneity.","authors":"Yakun Yang, Haohao Gao, Zhifei Fu, Weiying Hu, Yijing Li, Haixia Li, Hanqing Lin, Aodi Fan, Ke Yang, Jingyu Ni, Guanwei Fan, Lan Li","doi":"10.1186/s13020-026-01456-3","DOIUrl":"10.1186/s13020-026-01456-3","url":null,"abstract":"<p><strong>Background: </strong>Heart failure with preserved ejection fraction (HFpEF) has currently emerged as a predominant and challenging subtype of heart failure, with high morbidity and mortality. However, the efficacy of current therapeutic strategies for HFpEF remains unsatisfactory. The traditional Chinese medicine formulation Shenfu Qiangxin pill (SFQX) ameliorates clinical symptoms in patients with heart failure, but its precise mechanisms for HFpEF remain to be elucidated. This study aimed to investigate the therapeutic potential of SFQX for HFpEF and to elucidate the mechanisms underlying its effects.</p><p><strong>Methods: </strong>UPLC-Q-TOF-MS/MS analysis was performed to identify the major active ingredients of SFQX. The HFpEF mouse model was established using a high-fat diet and an Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) to evaluate the therapeutic efficacy of SFQX. We employed an integrated approach combining single-cell RNA sequencing (scRNA-seq) with functional and molecular validation to characterize SFQX-induced changes in cardiac cellular composition, cell-state remodeling, and tissue-level phenotypes in HFpEF.</p><p><strong>Results: </strong>We show that SFQX exerts therapeutic effects against HFpEF by coordinately modulating maladaptive cardiac cell subsets. Specifically, SFQX was associated with reprogramming of pathogenic immune cell polarization, normalization of fibroblast state heterogeneity, enhanced endothelial metabolic adaptability, and restoration of lymphatic endothelial homeostasis. These multicellular changes were accompanied by improved cardiac structure and function, reduced fibrosis and inflammation, enhanced lymphatic drainage capacity, and alleviated myocardial edema.</p><p><strong>Conclusion: </strong>Our findings highlight the ability of SFQX, as a multicomponent agent, to precisely regulate the highly heterogeneous pathology of HFpEF at a network level. This work not only establishes a mechanistic link between holistic principles of traditional medicine and modern biology but also provides a novel theoretical basis for SFQX's efficacy in multifactorial diseases.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13383478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535017","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}