Chinese Medicine最新文献

{"title":"Why the same herb is not the same medicine: plant epigenetic and metabolic plasticity as a missing variable in Chinese medicine.","authors":"Tae Kyung Hyun","doi":"10.1186/s13020-026-01434-9","DOIUrl":"10.1186/s13020-026-01434-9","url":null,"abstract":"<p><p>Traditional Chinese medicine (TCM) standardization is largely based on chemical equivalence, yet achieving reproducible therapeutic efficacy remains challenging. This limitation reflects an implicit assumption that medicinal plants are chemically static materials, overlooking their nature as dynamically regulated biological systems. This commentary emphasizes plant epigenetic and metabolic plasticity as a missing dimension in current quality assessment strategies. Environmental and developmental factors can establish stable regulatory states through epigenetic mechanisms, including DNA methylation and histone modification, thereby shaping metabolic organization beyond immediate growth conditions. Because therapeutic efficacy emerges from coordinated metabolic networks, evaluation based solely on static chemical composition is inherently limited. I propose an epigenetically informed materia medica framework for next-generation quality assessment. By integrating dynamic metabolic signatures, such as metabolite relationships and pathway coordination, with epigenetic indicators of regulatory history, this approach redefines consistency as predictable functional performance rather than chemical uniformity. This perspective provides a biologically realistic foundation for improving reproducibility while aligning standardization with the systemic principles of herbal therapeutics.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13220459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053077","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":"Ureic clearance granule ameliorates chronic kidney disease by reshaping microbial dysbiosis via modulating bile acid metabolism.","authors":"Li-Min Liu, Yu-Lu Zhang, Jing-Teng Zhou, Qing-Qing Yu, Wan-Ying Zhang, Wen-Feng Wang, Shu-Dan Pang, Hua Miao, Ying-Yong Zhao","doi":"10.1186/s13020-026-01423-y","DOIUrl":"10.1186/s13020-026-01423-y","url":null,"abstract":"<p><strong>Background: </strong>Chronic kidney disease (CKD) is a highly prevalent global public health problem that inevitably leads to renal failure. Although renin-angiotensin system blockers, as first-line therapy, can reduce proteinuria, they cannot prevent the progression to end-stage renal disease. Therefore, the development of new treatment strategies is urgently required. The uremic clearance granule (UCG) was widely used in patients with CKD. However, the underlying molecular mechanisms of UCG for CKD treatment remain unclear.</p><p><strong>Methods: </strong>Fecal gut microbiota and serum metabolites were analyzed using metagenomics and metabolomics, respectively. The expression of extracellular matrix components, Takeda G protein-coupled receptor 5 (TGR5), glucagon-like peptide-1 receptor (GLP-1R), and nuclear factor kappa B (NF-κB) p65 was examined by in adenine-induced CKD rats.</p><p><strong>Results: </strong>UCG improved renal function and alleviated kidney fibrosis in adenine-induced CKD rats. Mechanistically, significantly altered gut bacteria, including Helicobacter hepaticus, Gemella hemolysans, Bacteroides ovatus, Lactococcus cremoris, Bacteroides fragilis, Alistipes finegoldii, and Eubacterium limosum, showed strong linear correlations with serum creatinine levels in CKD rats. UCG treatment improved aberrant changes in these gut bacteria, indicating that UCG can reshape gut microbiota dysbiosis. Microbial-derived metabolites act as a bridge between gut microbiota and host. Further analysis showed that serum bile acids, including ursodeoxycholic acid (UDCA), taurodeoxycholic acid, and hyodeoxycholic acid (HDCA), were strongly correlated with serum creatinine levels in CKD rats, and these aberrant metabolites were reversed by UCG treatment. Notably, both UDCA and HDCA showed strong linear correlations with Bacteroides ovatus, Lactococcus cremoris, Bacteroides fragilis, and Eubacterium limosum, suggesting that UCG regulates microbial-derived metabolites. Moreover, UCG treatment upregulated protein expression of TGR5, GLP-1R, and downregulated NF-κB p65 protein expression in the kidney tissues of CKD rats, indicating that renoprotective effects of UCG are associated with modulation of microbial dysbiosis, regulation of bile acid metabolism and improvement of TGR5, GLP-1R, and NF-κB signaling.</p><p><strong>Conclusions: </strong>This study is the first to demonstrate that UCG ameliorates CKD and renal fibrosis by reshaping microbial dysbiosis and microbial-derived bile acid metabolism. Altered gut microbiota and metabolites may serve as biomarkers to evaluate efficacy of UCG. UCG may exert its renoprotective effects by enhancing TGR5, GLP-1R, and NF-κB p65 expression through regulating microbial dysbiosis-mediated bile acid metabolism.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13220541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053076","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":"Celastrol ameliorates atherosclerosis by inhibiting TLR4/STAT3/NLRP3-mediated macrophage pyroptosis.","authors":"Yaning Shi, Ziyi Li, Qizhi Liu, Yun Qiu, Junpeng Long, Qiong Yang, Chanjuan Zhang, Yongzhen Gong, Li Qin","doi":"10.1186/s13020-026-01430-z","DOIUrl":"10.1186/s13020-026-01430-z","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis is a chronic inflammatory disease characterized by plaque formation. Macrophage pyroptosis critically contributes to the formation and expansion of necrotic core as well as the instability of atherosclerotic plaque. Celastrol is a pentacyclic triterpene derived from the root of Tripterygium wilfordii Hook F, which has powerful anti-inflammatory properties. This study aimed to explore the effect and mechanism of celastrol in preventing atherosclerosis by regulating macrophage pyroptosis.</p><p><strong>Methods: </strong>An atherosclerotic mouse model in vivo and a macrophage pyroptosis model induced by ox-LDL in vitro were established successfully. The cell viability was examined by CCK-8. The role of pyroptosis was detected by transmission electron microscopy, LDH assay, and PI staining. HE staining assay was applied to evaluate the morphology of vascular tissues. The degree of lipid accumulation in plaques was measured using Oil Red O staining. The collagen content of plaques was detected using Masson staining. Western blot analysis, RT-qPCR, immunofluorescence staining, and immunohistochemistry were used to determine the levels of key proteins related to pyroptosis in macrophages. The underlying target of celastrol was investigated by CETSA and SPR assays.</p><p><strong>Results: </strong>Ox-LDL effectively activated macrophage pyroptosis, which was markedly inhibited by celastrol in vitro. Consistently, celastrol suppressed atherosclerotic plaque progression and instability in apoE^-/- mice by reducing macrophage pyroptosis in vivo. Mechanistically, celastrol could reduce the phosphorylation and nuclear translocation of STAT3 by targeting and inhibiting TLR4, thereby reducing the activation of NLRP3 inflammasomes and preventing macrophage pyroptosis.</p><p><strong>Conclusion: </strong>The present study demonstrates for the first time that celastrol prevents macrophage pyroptosis by inhibiting TLR4/STAT3/NLRP3 signaling pathway, ultimately alleviating atherosclerosis. These findings indicate that celastrol can serve as a potential therapeutic drug for atherosclerosis.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13217949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053071","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":"Licoisoflavone A potentiates oxaliplatin efficacy in colorectal cancer by dual targeting arginine metabolism of tumor microenvironment and cancer cells.","authors":"Lu Wang, Qing-Rui Liu, Bing-Wen Zhou, Chu-Yue Huang, Ping-Gang Ding, Yu-Jing Dong, Pu-Yang Gong, Zheng-Xin Chen, Zhi-Min Fan","doi":"10.1186/s13020-026-01428-7","DOIUrl":"10.1186/s13020-026-01428-7","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, with resistance to oxaliplatin (Oxa) and its associated side effects posing major therapeutic challenges. Natural flavonoids have shown potential in the prevention and treatment of CRC.</p><p><strong>Purpose: </strong>This study aimed to investigate whether combining Oxa with the bioactive flavonoid licoisoflavone A (LA) derived from Glycyrrhiza species could exert enhanced antitumor effects against CRC and to explore the underlying mechanisms.</p><p><strong>Methods: </strong>A CT26 tumor-bearing mouse model was established to evaluate the therapeutic efficacy of Oxa in combination with LA in vivo. Mass spectrometry-based proteomics and metabolomics analyses were performed to identify differentially expressed proteins and metabolites between the Oxa group and the Oxa plus LA group. Differential expressed proteins and associated pathways were subsequently validated in HCT116 cells, SW480 cells, and patient-derived organoids. Furthermore, two complex organoid models-an organoid-lymphocyte co-culture system and an air-liquid interface organoid system-were developed to investigate the underlying mechanisms. Flow cytometry and Western blot analyses were employed in both in vitro and in vivo settings.</p><p><strong>Results: </strong>The combination of LA and Oxa significantly inhibited tumor growth in CT26 tumor-bearing mice. Arginine metabolism was significantly reduced following LA treatment. Arginase-1 (ARG1) was identified as a potential target of LA. LA significantly downregulated ARG1 expression, which was associated with an increased proportion of CD8⁺ T cells and reduced expression of CD69⁺ and PD-1, suggesting a potential alleviation of T cell exhaustion-related features. Moreover, LA inhibited CRC cell proliferation by suppressing ARG1-mediated activation of the PI3K/Akt/mTOR signaling pathway.</p><p><strong>Conclusions: </strong>LA is a natural flavonoid that targets arginine metabolism and enhances the therapeutic efficacy of Oxa in CRC treatment.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13217967/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053075","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":"Homo- and hetero-dimeric sesquiterpenoids with unprecedented skeletons and their co-occurring monomers from Vernonia solanifolia with anti-liver steatotic potential.","authors":"Yue Yang, Fei Zhou, Chang-Qiang Ke, Sheng Yao, Ligen Lin, Chunping Tang, Yang Ye","doi":"10.1186/s13020-026-01418-9","DOIUrl":"10.1186/s13020-026-01418-9","url":null,"abstract":"<p><strong>Background: </strong>Sesquiterpenoids show potential as therapeutics against metabolic dysfunction-associated steatotic liver disease (MASLD). Vernonia solanifolia Benth. has been traditionally used to treat abdominal pain and enteritis. However, the anti-steatotic effect of V. solanifolia and its chemical principles have not been illustrated.</p><p><strong>Methods: </strong>The structures of new compounds were determined through extensive spectroscopic analysis including 1D/2D nuclear magnetic resonance (NMR), high-resolution electrospray ionization mass spectrometry, ultraviolet and infrared. Especially, the structure of compound 6 was further verified by single crystal X-ray diffraction, and the relative and absolute configurations of compounds 1-5 and 7-9 were resolved with the help from density-functional theory-NMR and time-dependent density-functional theory-electronic circular dichroism calculation. The lipid-lowering activity was evaluated on palmitic acid/oleic acid (P/O)-treated AML12 hepatocytes. The biological evaluation was performed using Nile Red staining, flow cytometry, commercial kits, and Western blotting.</p><p><strong>Results: </strong>Nine new sesquiterpenoid dimers and their co-occurring monomers (1-9) were identified from the leaves of V. solanifolia. A unique 10/5/6/5/7 pentacyclic ring system is exemplified in compounds 1 and 2. These compounds were constructed from a germacranolide and a 4,5-seco-guaianolide monomer through an unprecedented spiro cyclohexene ring. The first examples of germacrane-guaiane and guaiane-xanthane heterogeneous dimers are shown in compounds 3 and 4, respectively, which also possess a spiro cyclohexene ring linkage. A guaianolide dimer featuring a rare C-13/C-13' linkage is exhibited in compound 5. The plausible biosynthetic pathways for compounds 1 and 5 were proposed. The isolates were tested for their lipid-lowering effect on P/O-treated AML12 hepatocytes, and the results showed that compound 3 significantly reduced lipid content in hepatocytes by triggering the AMP-activated protein kinase/acetyl-CoA carboxylase/peroxisome proliferator-activated receptor γ coactivator-1α signaling pathway.</p><p><strong>Conclusion: </strong>Five homo- and hetero-dimeric sesquiterpenoids with unprecedented skeletons were characterized from V. solanifolia, together with four new co-occurring monomers. It's the first time to report the lipid-lowering activity of sesquiterpenoids from this genus, which might be developed as lead compounds against MASLD.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13217702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053073","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":"Targeting the gut‒kidney axis for lupus nephritis treatment: multimechanism regulatory strategies and evidence from Traditional Chinese medicine.","authors":"Qingyun Fang, Jiabao Liu, Chen Xuan, Chaofan Li, Xin Jiang, Shuangna Zhang, Qinggang Li, Xiaomin Liu, Qun Liu, Li Zhang, Yong Wang, Jing Cui, Yilun Qu, Jie Zhang, Ping Li, Xiangmei Chen","doi":"10.1186/s13020-026-01426-9","DOIUrl":"10.1186/s13020-026-01426-9","url":null,"abstract":"<p><p>Lupus nephritis (LN) treatment remains challenging because of the limited efficacy and substantial side effects of conventional immunosuppressive therapies. Traditional Chinese medicine (TCM), with its holistic and multitarget approach, offers unique therapeutic potential. The emerging gut-kidney axis theory provides a new framework for understanding LN pathogenesis by linking gut dysbiosis and intestinal barrier injury to renal inflammation. This review systematically examines the role of gut-kidney axis dysregulation in LN progression and establishes connections between the TCM spleen-kidney correlation theory and this modern concept. Accumulating evidence suggests that TCM compounds and active ingredients alleviate renal injury and improve LN through multiple mechanisms. TCM compounds modulate the gut microbiota composition, enhance intestinal barrier integrity, reduce endotoxin translocation, and suppress systemic inflammation. These findings position the gut-kidney axis as a critical target for TCM intervention. Through multicomponent synergy, TCM restores gut homeostasis and inhibits aberrant immune responses. Future studies should integrate multiomics approaches, including metagenomics and metabolomics, and prospective clinical trials should dynamically track the gut microbiota and metabolite profiles in LN patients. Such investigations will clarify the precise mechanisms by which TCM modulates the gut-kidney axis and facilitate the development of personalized TCM-based therapeutic strategies.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13214132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148041239","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":"6-Shogaol inhibits HSCs activation and liver fibrosis by regulating glycolytic reprogramming via targeting HIF-1α.","authors":"Junfa Yang, Min Shu, Hui Fang, Fan Yang, Jiahe Li, Yuansong Sun, He Li, Tao Xu","doi":"10.1186/s13020-026-01396-y","DOIUrl":"10.1186/s13020-026-01396-y","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Liver fibrosis is a representative scarring response that can ultimately lead to liver cancer. However, relevant antifibrotic drugs for the effective treatment of liver fibrosis in humans have not yet been identified. 6-Shogaol is derived from natural products and exhibits multiple biological activities, including anti-inflammatory and antioxidant properties; however, its efficacy and potential mechanism of action against liver fibrosis remains unclear. This study aimed to examine the anti-fibrotic properties and potential mechanisms of action of 6-Shogaol.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Two liver fibrosis mouse models (carbon tetrachloride (CCl&lt;sub&gt;4&lt;/sub&gt;) and bile duct ligation (BDL)) were constructed to evaluate the anti-fibrotic properties of 6-Shogaol in vivo. Transforming growth factor-β1 (TGF-β1)-induced human hepatic stellate cells (HSCs) LX-2 cells were used as in vitro models. Network pharmacology analysis was introduced to explore the key targets of 6-Shogaol regarding the mechanisms on liver fibrosis. Molecular docking, molecular dynamics simulations, drug affinity reactivity target stability (DARTS) and isothermal titration calorimetry (ITC) were used to detect the affinity and binding between 6-Shogaol and its target. Additionally, we invested the mechanism of 6-Shogaol through RNA sequencing combined with Western blotting, oxygen consumption rate (OCR), extracellular acidification rate (ECAR), immunofluorescence co-localization, histopathology, immunohistochemical staining and RT-qPCR.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The results showed that 6-Shogaol remarkably alleviated CCl&lt;sub&gt;4&lt;/sub&gt;- and BDL-induced liver fibrosis in mice, including observations of improved liver function, decreased activity of HSCs, and decreased extracellular matrix (ECM) deposition. In an in vitro model, 6-Shogaol suppressed TGF-β1-induced LX-2 activation. Mechanistically, RNA sequence analysis revealed that the effect of 6-Shogaol on liver fibrosis is linked to glycolytic reprogramming. 6-Shogaol suppressed HSCs glycolysis by decreasing glycolytic enzymes (HK2, PKM2, and GLUT1) and glycolytic metabolite levels (lactic acid and pyruvic acid). Furthermore, network pharmacology suggested HIF-1α as a potential 6-Shogaol target. Molecular docking, molecular dynamics simulations, DARTS, and ITC confirmed that 6-Shogaol could directly bind to HIF-1α. Interestingly, we demonstrated that HIF-1α knockout significantly inhibited HSCs glycolysis and activation, whereas the overexpression of HIF-1α increased HSCs glycolysis and activation. Moreover, specific knockout of HIF-1α did not enhance the suppressive effect of 6-Shogaol on HSCs activation or fibrosis-associated protein expression in vivo.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;These findings showed that 6-Shogaol ameliorated liver fibrosis by modulating the expression of HIF-1α associated with glycolysis reprogramming and validate 6-Shogaol as a promising therapeutic strategy for l","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13214082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148041236","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":"Epigenetic precision diagnostics of traditional Chinese medicine (TCM) syndrome differentiation: a pilot study of atrial fibrillation with qi-yin deficiency syndrome based on 5-hydroxymethylcytosine signatures in extracellular vesicle DNA from plasma.","authors":"Shaowei Fan, Haoyu Chen, Hangyu Chen, Bai Du, Baixin Zhen, Xianglong Chen, Lei Zhang, Xiaxuan Li, Maimaitiyasen Duolikun, Long Chen, Han Gao, Shuqing Shi, Xiaohan Zhang, Yangang Wang, Yuanhui Hu, Jian Lin","doi":"10.1186/s13020-025-01267-y","DOIUrl":"10.1186/s13020-025-01267-y","url":null,"abstract":"<p><strong>Background: </strong>Syndrome differentiation in Traditional Chinese Medicine (TCM) is pivotal to clinical practice and dictates the efficacy of medicinal treatments. However, precision diagnostic models for TCM syndromes, constructed from biomarkers such as metabolites and proteins, have failed to achieve high precision. Recent studies have highlighted a strong link between TCM and epigenetics, an area that remains largely unexplored in TCM diagnosis. Taking atrial fibrillation (AF) with Qi-Yin deficiency syndrome (QYDS) as an example, we utilized a type of epigenetic sequencing technology called 5hmC-Seal and integrated it with various machine learning models to develop an Epigenetic Differential Syndrome (Epi-DS) technology for identifying epigenetic biomarkers. This approach is crucial for developing more accurate diagnostic models for traditional Chinese medicine syndromes and for advancing the modernization of traditional Chinese medicine.</p><p><strong>Methods: </strong>In this study, we conducted a single-center, prospective study involving two independent cohorts (cohort 1 and cohort 2) in AF, including QYDS and non-Qi-Yin deficiency syndrome (NQYDS). Next, we utilized 5hmC-Seal to obtain the patients' 5hmC genome-wide profiles in plasma extracellular vesicles DNAs (evDNAs). Meanwhile, a variety of sophisticated machine learning algorithms were employed across three datasets-training, validation, and external cohorts (the training and validation sets constituting cohort 1 and the external cohort constituting cohort 2) to construct and validate QYDS diagnosis model.</p><p><strong>Results: </strong>Based on the hydroxymethylation profile of the QYDS in AF, we have successfully constructed a disease-phenotype-molecule biological network for AF. At the molecular level, we identified nine characteristic 5hmC markers for the QYDS in AF and successfully established a diagnostic model for this syndrome. In Cohort 1's training set, the area under the receiver operating characteristic curve (AUC) was as high as 0.984, with a sensitivity of 0.976 and a specificity of 1.000. In validation set, the AUC was 0.949, with a sensitivity of 0.952 and a specificity of 0.952. In the independent external validation cohort 2, the AUC was as high as 0.934, with a sensitivity of 0.886 and a specificity of 0.919. Moreover, the diagnostic model we built based on symptoms and molecular markers achieved an AUC value of 0.864 in an independent external cohort.</p><p><strong>Conclusions: </strong>A novel precision diagnostic approach of TCM Syndrome Differentiation was established based on Epi-DS. The disease-phenotype-molecule network we have constructed reveals the epigenetic foundation of TCM and has identified molecular diagnostic markers for the QYDS in AF. This provides an example for understanding the molecular basis of TCM syndrome differentiation and for integrated traditional Chinese and Western medicine diagnosis.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13214416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148041294","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 prevents CUMS induced depressive-like behaviors by inhibiting microglia-mediated synaptic pruning induced by gut dysbiosis.","authors":"Lu Zhang, Jingyi Quan, Linlin Nie, Shenglan He, Yeze Lin, Xiaoxiao Liu, Yifan Zhang, Lixing Zhuang, Chao Jia, Min Li, Qi Wang, Lining Duan","doi":"10.1186/s13020-026-01422-z","DOIUrl":"10.1186/s13020-026-01422-z","url":null,"abstract":"<p><strong>Rationale: </strong>Electroacupuncture (EA) has been widely used for depression treatment. Microbiota-gut-brain (MGB) axis plays a vital role in regulating emotional behaviors. However, the potential role of MGB axis in EA-mediated protective effects remains unclear.</p><p><strong>Methods: </strong>The protective effects of EA in chronic unpredictable mild stress (CUMS) induced mice were evaluated, and the gut microbiota and metabolic profiles were analyzed. Fecal microbiota transplantation (FMT) was utilized to explore the role of MGB axis in the protective effects of EA. Analyses related to synaptic pruning mediated by microglia were conducted to explore the molecular mechanisms.</p><p><strong>Results: </strong>In this study, EA treatment prevented depressive-like behaviors in CUMS mice. Mechanistically, EA ameliorated CUMS-induced gut microbiota dysbiosis and inflammation, and partially restored gut microbial metabolism, particularly affecting the abundance of Alistipes and taurine metabolism. Furthermore, EA significantly reduced systemic and hippocampal inflammation. It also attenuated aberrant synaptic pruning in the hippocampus. Moreover, FMT from CUMS mice induced depressive-like behaviors, gut inflammation and microglia-mediated aberrant synaptic pruning, whereas FMT from EA-treated donors exerted protective effects against these impairments.</p><p><strong>Conclusion: </strong>Collectively, our findings suggest that EA prevented CUMS-induced depression-like behaviors and support the involvement of the MGB axis in its protective effects.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13202871/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027736","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":"Research advances in the application of betulinic acid for anti-inflammatory and anti-tumour therapy.","authors":"Zewen Chu, Shuaiyu Jiang, Yuting Li, Xiang Li, Wan Xin Koh, Pottakorn Aruncharoenphonchai, Yue Ding, Yanwei Xiang","doi":"10.1186/s13020-026-01424-x","DOIUrl":"10.1186/s13020-026-01424-x","url":null,"abstract":"<p><p>Betulinic acid (BA) is a naturally occurring pentacyclic triterpenoid widely distributed in a variety of medicinal plants and has attracted considerable attention as an active constituent of several traditional herbal medicines. In recent years, research on BA has increasingly focused on cancer and inflammation owing to its broad-spectrum pharmacological activities against tumours and inflammation-related diseases. This review summarizes recent advances in the study of BA and its derivatives, with particular emphasis on their antitumour and anti-inflammatory properties, underlying molecular mechanisms, and strategies to improve therapeutic efficacy. Accumulating evidence indicates that BA exerts its antitumour and anti-inflammatory effects through multiple pathways and molecular targets. In addition, representative structural modification approaches and nano-enabled drug delivery strategies developed to overcome the intrinsic limitations of BA, such as poor aqueous solubility and low bioavailability, are systematically discussed. Finally, key challenges associated with the clinical translation of BA are highlighted from a translational perspective, with the aim of providing references for further experimental investigations and clinical development. Overall, BA represents a promising bioactive monomer with dual anti-tumour and anti-inflammatory potential, particularly in the context of inflammation-associated cancers. CONCLUSIONS: The research and development prospects of BA and its derivatives as active monomeric compounds in traditional Chinese medicine are promising, yet several challenges remain. In terms of research directions, further structural optimization of these derivatives is needed to enhance their biological activity, selectivity, and pharmacokinetic properties. In addition, exploring new targets and mechanisms of action represents another important avenue, which may provide a more solid theoretical and experimental foundation for the development of BA as a new anti-tumour and anti-inflammatory drug.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13202815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027749","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}