Chinese Medicine最新文献

{"title":"Polygala oligosaccharide esters improve memory disorder by restoring gut microbiota homeostasis through the regulation of the \"gut-brain\" axis.","authors":"Yan Wang, Chaoyun Ren, Wenkai Dong, Qiule Li, Fanying Deng, Fuxia Zhao, Yangang Cheng, Peng Sun, Huifang Li, Yingli Wang","doi":"10.1186/s13020-026-01436-7","DOIUrl":"10.1186/s13020-026-01436-7","url":null,"abstract":"<p><strong>Background: </strong>Yuanzhi (Polygala tenuifolia Willd.) possesses the effects of calming the spirit, enhancing intelligence, regulating the heart-kidney connection, eliminating phlegm, and reducing swelling. It is commonly used in the treatment of insomnia and forgetfulness. Previous studies have indicated that the oligosaccharide esters (OE) derived from Yuanzhi exhibit neuroprotective and memory-enhancing activities. However, its underlying mechanisms, particularly those involving the gut-brain axis, remain unclear.</p><p><strong>Purpose of the research: </strong>This study aimed to investigate the therapeutic efficacy and underlying mechanisms of Oligosaccharide Esters (OE) from Polygala tenuifolia Willd. against memory dysfunction in mice, with a specific focus on the gut-brain axis.</p><p><strong>Methods: </strong>A mouse model of memory dysfunction was induced using D-galactose combined with AlCl₃. Behavioral tests, molecular biology techniques (histopathology, enzyme-linked immunosorbent assay (ELISA), immunohistochemistry, and Western blot), and multi-omics approaches (16S rRNA sequencing and lipidomic analysis) were employed to investigate the therapeutic efficacy of OE against memory dysfunction. Meanwhile, with the aid of fecal microbiota transplantation (FMT) assay, we observed the repair of brain and colonic tissues, inflammatory responses and intestinal permeability, further clarified the regulatory effect of OE on gut microbiota, and ultimately revealed the underlying mechanisms of OE mediated by the gut-brain axis.</p><p><strong>Results: </strong>OE administration significantly enhanced learning and memory in MD mice, repaired neuronal damage in the hippocampal regions (CA1, CA3, DG) of the MD mouse brain, and increased the number of Nissl bodies. OE elevated the serum levels of BDNF and CREB and reduced the TMAO level; simultaneously, it enhanced the activities of SOD and GSH-Px and decreased the MDA content in the brain tissue. OE treatment modulated the relative abundance of the gut microbiota in MD mice, restored the microbial imbalance induced by memory deficits, and particularly affected the abundances of Firmicutes, Bacteroidetes, their ratio (F/B), and genera such as Ligilactobacillus. Lipidomics analysis indicated that OE exerts its therapeutic effects primarily by regulating the glycerophospholipid metabolism pathway, and a total of 17 key differential lipid metabolites were identified. Correlation analysis further revealed that the levels of key differential lipid metabolites, LysoPC(22:2) and PC(38:4), were significantly positively correlated with the levels of neuroprotective factors (CREB, BDNF) and the activities of antioxidant enzymes (SOD, GSH-Px), but were significantly negatively correlated with the harmful metabolite TMAO and the oxidative damage product MDA. In contrast, the lipid metabolite GPEA exhibited a trend opposite to that of LysoPC(22:2) and PC(38:4). Further investigation results demonst","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204237","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":"Chuangling Ye mitigates diabetic foot ulcer through suppressing keratinocyte ferroptosis via inhibiting ACSS2/ACSL4 axis.","authors":"Xiao Feng, Nan Yi, Cunyu Zhang, Liang Tang, Xindong Yin, Ya Zhao, Taiyang Zhu, Jianhua Zhu, Qian Feng, Weiwei Chen, Yawen Xia, Chaoqun Ma","doi":"10.1186/s13020-026-01435-8","DOIUrl":"10.1186/s13020-026-01435-8","url":null,"abstract":"<p><strong>Background: </strong>Diabetic foot ulcers (DFU) is a serious complication of diabetes, and keratinocyte ferroptosis has been shown to accelerate its pathological progression. Chuanglin Ye (CLY), widely used in clinical practice for the treatment of DFU, has been reported to exert anti-inflammation effects and promote skin regeneration. However, its pharmacological mechanisms on DFU remain unclear.</p><p><strong>Methods: </strong>The DFU rats were treated with CLY (0.225 and 0.45 g/mL) for 21 days to evaluate its therapeutic efficacy. The chemical composition of CLY was analyzed using UPLC-MS/MS. Network pharmacology, western blot, and immunohistochemical staining were performed to assess the anti-ferroptosis effects of CLY. To validate the protective role of CLY against ferroptosis, RSL3, a ferroptosis inducer, was applied in this study. Subsequently, HaCaT cells were exposed to advanced glycation end products (AGEs) to establish an in vitro model of keratinocyte ferroptosis, further confirming the inhibitory effects of CLY on ferroptosis. RNA sequencing was conducted to elucidate the molecular mechanisms underlying CLY-mediated protection against keratinocyte ferroptosis. The functional involvement of the ACSS2/ACSL4 axis was verified through plasmid-mediated gene overexpression in vitro. Molecular docking analysis was employed to identify potential bioactive compounds in CLY that target ACSS2.</p><p><strong>Results: </strong>CLY administration significantly accelerated wound healing in DFU rats. Network pharmacology analysis indicated the regulation of ferroptosis underlies the therapeutic effect of CLY against DFU, which was further supported by its ability to ameliorate lipid peroxidation and iron overload. In contrast, the ferroptosis inducer RSL3 attenuated the protective effects of CLY in DFU rats. In vitro, CLY markedly suppressed AGEs-induced lipid peroxidation and excessive ROS level. Mechanistically, RNA-seq analysis and subsequent validation experiments revealed the anti-ferroptosis effect of CLY depends on the inhibition of ACSL4 acetylation in keratinocytes. Furthermore, ACSS2 was identified as a key protein promoting ACSL4 acetylation, which was inhibiting by CLY. Finally, six major compounds in CLY were identified as active constituents targeting ACSS2.</p><p><strong>Conclusion: </strong>Our findings demonstrate CLY promotes DFU wound healing by inhibiting keratinocyte ferroptosis through suppressing ACSS2-mediated ACSL4 acetylation, highlighting its potential as a rational therapeutic approach for the management of DFU.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204171","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":"An integrated machine learning framework for TCM five-flavor classification based on E-tongue profiling and SHAP analysis.","authors":"Ziang Li, Xianglong Meng, Lin Yang, Xiaoning Yan, Liangting Li, Yiwei Fu, Jingjing Tang, Shuosheng Zhang","doi":"10.1186/s13020-026-01399-9","DOIUrl":"10.1186/s13020-026-01399-9","url":null,"abstract":"<p><strong>Background: </strong>The \"five-flavor\" (wu wei) classification is a core organizing principle in Traditional Chinese Medicine (TCM) pharmacology and quality control, yet its assessment still relies on subjective organoleptic evaluation, limiting standardization and reproducibility.</p><p><strong>Methods: </strong>Eighty-four processed herbal slices were analyzed using an electronic tongue to obtain multichannel sensor response profiles. Based on these data, we developed a dual-strategy ensemble learning framework in which a heterogeneous stacking model was trained for five-flavor identification while a voting ensemble was established in parallel for intensity grading. Model interpretability was evaluated using SHapley Additive exPlanations (SHAP) to quantify feature contributions and to relate prediction outcomes to specific electrochemical response patterns.</p><p><strong>Results: </strong>On the independent test set, the stacking ensemble showed moderate and flavor-dependent classification performance, with a macro-AUC of 0.876 and a balanced accuracy of 0.629. Discriminative performance was higher for Bitter and Sweet than for Sour, Salty, and Pungent. Full-stack SHAP analysis further identified P_13 and P_8 as the most influential features overall, with P_13 contributing mainly to the discrimination of bitter and pungent attributes, whereas P_8 was more strongly associated with sour, salty, and sweet characterization.</p><p><strong>Conclusions: </strong>This study demonstrates a data-driven workflow for digitizing TCM five-flavor assessment. Further validation with expanded sample sizes and chemical corroboration of sensor attributions is needed before operational deployment.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13235049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161992","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":"Unveiling medication patterns in traditional Chinese medicine for the prevention of colorectal cancer recurrence: from potential combinations to validation of components and targets.","authors":"Qianqian Bu, Shaoxun Yuan, Xiaoman Wei, Junyi Wang, Liu Li, Pan Chen, Weixing Shen, Dongdong Sun, Lingyu Linda Ye, Yun Yang, Luying Xu, Sicheng Lu, Dayue Darrel Duan, Haibo Cheng","doi":"10.1186/s13020-026-01438-5","DOIUrl":"10.1186/s13020-026-01438-5","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a prevalent malignant tumor with high incidence and mortality rates, with recurrence being the primary cause of death among patients. Traditional Chinese Medicine (TCM) utilizes a holistic cognitive approach to develop herbal treatment strategies, displaying significant efficacy in slowing tumor progression and improving patients' quality of life. However, discrepancies in herbal prescription strategies arise from variations in clinicians' syndrome differentiation and experiential knowledge, leading to a lack of systematic understanding of compound prescription compatibility rules. This study aims to identify TCM prescriptions that are effective in preventing or treating CRC recurrence through evidence-supported and clinically applied prescriptions. By employing Apriori association rule mining and graph convolutional network analysis, a core herb spectrum associated with anti-recurrence prescriptions was identified, emphasizing a high-confidence herbal combination for further mechanistic exploration. Subsequent network pharmacology analysis revealed quercetin and kaempferol as representative active compounds with PTGS2 identified as a potential key target. Molecular docking, molecular dynamics simulation, public database analysis, and in vitro experiments provided initial evidence supporting their interaction and biological effects in CRC cells. Overall, this study reveals the compatibility characteristics of TCM prescriptions for preventing CRC recurrence and offers a scientific foundation for the continued use of TCM-based strategies in managing CRC recurrence.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13235114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161967","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":"Hyperoside protects against poly-GR-mediated neurodegeneration via regulation of mitochondrial fission and oxidative stress in C9orf72-associated ALS.","authors":"Wen-Chi Hsieh, Chun-Yu Lin, Hsuan-Cheng Wu, Eddie Feng-Ju Weng, Shao-Ming Wang","doi":"10.1186/s13020-026-01433-w","DOIUrl":"10.1186/s13020-026-01433-w","url":null,"abstract":"<p><strong>Background: </strong>Arginine-rich poly-glycine-arginine (poly-GR), a toxic dipeptide repeat protein generated from C9orf72 hexanucleotide repeat expansion, drives mitochondrial dysfunction, oxidative stress, and neuronal loss in amyotrophic lateral sclerosis (ALS). Hyperoside, a bioactive flavonoid, exhibits antioxidant and cytoprotective properties, but its therapeutic relevance to C9orf72-associated ALS remains unclear.</p><p><strong>Purpose: </strong>To determine whether hyperoside attenuates poly-GR-induced mitochondrial and oxidative injury and improves neuronal survival in cellular and animal models of C9orf72-ALS.</p><p><strong>Methods: </strong>A combined in vitro and in vivo experimental study using motor neuron-like cells and an AAV-mediated neonatal mouse model of poly-GR toxicity. NSC34 cells expressing EGFP-GR₅₀ were analyzed for mitochondrial morphology, membrane potential, ROS generation, antioxidant signaling, and apoptosis using confocal microscopy, CellROX/MitoTracker assays, Western blot analysis, and viability testing. For in vivo assessment, neonatal mice received intracerebroventricular AAV9-EGFP-GR50 followed by intraperitoneal hyperoside (10 mg/kg). Survival, cerebral hemisphere length, and cortical NeuN⁺ neuron numbers were quantified.</p><p><strong>Results: </strong>Poly-GR expression induced pronounced mitochondrial fragmentation, reduced membrane potential, elevated ROS, and suppressed Nrf2/HO-1/GPx4 signaling, accompanied by increased Drp1 and reduced Opa1 expression. Hyperoside reversed these abnormalities by restoring mitochondrial integrity, normalizing the Drp1/Opa1 balance, enhancing Nrf2 nuclear accumulation, and increasing the expression of HO-1 and GPx4. Hyperoside also reduced cleaved caspase-3 and corrected the Bax/Bcl-2 ratio, improving cell viability under basal and oxidative stress conditions. In vivo, hyperoside modestly prolonged survival, increased cerebral hemisphere length, and significantly preserved cortical neuronal numbers in AAV9-EGFP-GR₅₀ mice.</p><p><strong>Conclusion: </strong>Hyperoside mitigates poly-GR-induced neurotoxicity by alleviating excessive mitochondrial fission, strengthening Nrf2-dependent antioxidant defenses, and suppressing apoptosis. These findings support hyperoside as a promising multi-target therapeutic candidate for C9orf72-associated ALS.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13235191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148162011","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":"Metapath2vec and attention-driven heterogeneous graph learning for prioritizing TCM-derived small molecules in gastric cancer.","authors":"Nengquan Sheng, Jinran Liu, Wen Fang, Caijie Zheng, Yinuo Ma, Yang Sun, Hongqi Chen","doi":"10.1186/s13020-026-01431-y","DOIUrl":"10.1186/s13020-026-01431-y","url":null,"abstract":"<p><p>Traditional Chinese Medicine (TCM) represents a multi-component therapeutic system with substantial chemical complexity. This complexity makes it difficult to directly elucidate anti-gastric cancer mechanisms from macroscopic herbal formulae. To support the systematic prioritization of potential small-molecule candidates, this study focuses on screening bioactive small-molecule constituents from TCM. We constructed a heterogeneous network integrating Chinese herbal pieces (CHPs), Chinese patent medicines (CPMs), genes, diseases, and small molecules, and incorporated metapath2vec representations and attention mechanisms into a graph neural network framework, the model is designed to learn relational patterns among heterogeneous nodes. Network pharmacology and in vitro validation in AGS and MKN-45 gastric cancer cell lines show that Icaritin and Arundine inhibit cell proliferation and induce apoptosis. This study presents an AI-assisted pipeline for candidate prioritization, providing methodological support for the systematic prioritization and preliminary validation of bioactive TCM molecules in gastric cancer.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148155538","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":"Gambogic acid induces cell death via covalent binding with PRDX1 to regulate ER stress and autophagy.","authors":"Jinyan Wang, Wei Zhang, Li Yang, Xiaoru Zhong, Jinhuan Ou, Ashok Iyaswamy, Xin Gu, Chuanbin Yang, Bing Guo, Mingjun Shi, Jigang Wang","doi":"10.1186/s13020-025-01144-8","DOIUrl":"10.1186/s13020-025-01144-8","url":null,"abstract":"<p><strong>Background: </strong>Gambogic acid (GA) is a natural bioactive compound derived from Garcinia hanburyi Hook. F, has proven anticancer activity and is currently in Phase II clinical trials for the treatment of cancer. However, the molecular mechanisms and targets underlying GA's anti-renal cell carcinoma effects remain unclear.</p><p><strong>Methods: </strong>CCK-8 assay evaluated kidney cancer cell viability via formazan formation. Flow cytometry identified apoptotic cells using characteristic fluorescence signals. Western blotting assessed autophagy- and apoptosis-related protein expression through extraction, SDS-PAGE, transfer, and antibody detection. JC-1 assay determined mitochondrial health by measuring red-to-green fluorescence ratio in kidney cancer cells. The production of reactive oxygen species (ROS) was quantified through CM-H2DCFDA staining. Additionally, a range of techniques, such as proteomics, activity-guided protein profiling (ABPP), and cellular thermal stability assays (CETSA), were employed to ascertain the molecular targets involved.</p><p><strong>Results: </strong>GA induces cell death by inducing ER stress and modulating autophagy. GA-induced autophagy is involved in ER stress activation. Importantly, GA-induced ER stress and subsequently cell death is caused by increased ROS levels. Mechanistic studies show that peroxiredoxin-1 (PRDX1), a key antioxidant enzyme, is a directly covalent binding target of GA, and overexpression of PRDX1 mitigates GA-induced ROS production and subsequently cell death.</p><p><strong>Conclusion: </strong>The study identified PRDX1 is a potential directly covalent binding protein of gambogic acid, and elucidated its mechanism for inducing cell death that involving in ROS-mediated ER stress and autophagy regulation. The results obtained offer fresh perspectives on the mechanisms underlying the cytotoxic effects induced by gambogic acid, further suggesting that PRDX1 may represent a promising candidate for targeted therapy in the development of novel anticancer agents, notably for the treatment of kidney cancer.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148155481","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":"A clinical and mechanistic study on traditional Chinese medicine herbs used in olfactory training.","authors":"Wei Zhang, Yingjian Liu, Jiahui Sun, Fei Wang, Licong Nie, Jinxin Chen, Hang Ren, Jiaxin Chen, Yu Zheng, Weihong Liu, Yonggang Liu","doi":"10.1186/s13020-026-01432-x","DOIUrl":"10.1186/s13020-026-01432-x","url":null,"abstract":"<p><strong>Background: </strong>Olfactory dysfunction (OD) is a prevalent condition with limited treatment options, severely impairing patients' quality of life. Olfactory training (OT) using conventional odorants provides limited benefit. Traditional Chinese Medicine (TCM) herbs with complex odors may offer novel OT agents, but their mechanism and clinical value remain unclear.</p><p><strong>Methods: </strong>In a prospective, open-label, parallel-controlled clinical observation, 73 OD patients (TCM-OT group: n = 36; control group: n = 37) received either 3-month TCM-based OT (6 herbs) or mometasone furoate nasal spray. Olfactory function was assessed by olfactory identification test (OIT), visual analog scale (VAS), and quality-of-life questionnaire (QOD). Volatile profiles of the six herbs were characterized by GC-MS. We then performed systematic functional screening of 16 major herb odorants and 4 common chemical odorants (eugenol, citronellal, phenylethyl alcohol, eucalyptol) against ~ 400 human olfactory receptors (hORs) using luciferase assays. Results were combined with public database entries (M2OR, OlfactionBase) to compare OR activation patterns. Molecular docking and molecular dynamics (MD) simulations were performed for (-)-Borneol, a representative active component, against its responsive ORs.</p><p><strong>Results: </strong>TCM-OT significantly improved the primary outcome (OIT) compared with control (mean improvement 11.31 ± 6.30 vs. 6.22 ± 4.99, p < 0.001, Cohen's d = 1.150). Secondary outcomes (VAS and QOD) showed trends favoring TCM-OT but did not reach statistical significance after Bonferroni correction. Greater benefit was observed in younger patients. Herb odorants displayed higher chemical diversity than chemical odorants. Functional screening identified 34 odorant-OR activation pairs for herb odorants (23 novel) and 11 pairs for chemical odorants (10 novel). Integrated analysis revealed that herb odorants collectively activated all 17 hOR families, whereas chemical odorants engaged only 8 families. Molecular simulations further elucidated the multi-receptor recognition mechanism of (-)-Borneol.</p><p><strong>Conclusions: </strong>TCM-OT is a promising multi-target approach for OD. The broad activation of all OR families by herb odorants - contrasting with the limited engagement of conventional chemical odorants - provides a molecular rationale for the efficacy of TCM-OT and guidance for the selection of olfactory agents used in OT.</p><p><strong>Trial registration: </strong>This study was retrospectively registered with the Eye Hospital of China Academy of Chinese Medical Sciences (YKEC-KT-2025-057-P002).</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13227741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148713","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":"Huayu-qutan formula ameliorates hypertrophic cardiomyopathy by regulating MAPK and HIF‑1α-signaling pathways.","authors":"Wei Ding, Ni Zhang, Lei Xiao, Le Yu, Tian-Shi Wu, Yuan-Jie Feng, Wei Chen","doi":"10.1186/s13020-026-01400-5","DOIUrl":"10.1186/s13020-026-01400-5","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Hypertrophic cardiomyopathy (HCM) is often complicated by coronary microvascular dysfunction (CMD), which precipitates localized myocardial ischemia and metabolic disturbance, triggering compensatory cardiomyocyte hypertrophy. This hypertrophy, in turn, exacerbates microvascular insufficiency, forming a pathological feedback loop and culminating in persistent cellular stress, inflammatory infiltration, and myocardial fibrosis. This \"ischemia-hypertrophy-inflammation-fibrosis\" interrelationship not only drives pathological remodeling but also significantly elevates the risk of heart failure, arrhythmias, and adverse prognosis. The traditional formula Huayu Qutan Formula (HYQT), used clinically for years, has been shown to significantly enhance cardiac function in HCM patients. However, its underlying mechanisms remain poorly elucidated. This study aims to explore HYQT's therapeutic effects on HCM and to reveal its intrinsic mechanisms.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Blood-absorbed constituents of HYQT were identified using UHPLC-MS, followed by network pharmacology analysis and molecular docking to predict potential targets and key signaling pathways. An isoproterenol (ISO)-induced HCM mouse model, along with parallel in vitro injury models using H9C2 cardiomyocytes and human cardiac microvascular endothelial cells (HCMECs), was established to systematically assess the in vivo and in vitro effects of HYQT. To comprehensively evaluate HYQT's modulation of myocardial hypertrophy, fibrosis, and angiogenesis, echocardiography, laser speckle perfusion imaging, immunohistochemistry, western blotting, reactive oxygen species (ROS) assays, and wound-healing assays were performed.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;UHPLC-MS analysis identified 31 blood-absorbed bioactive components of HYQT. Integrated network pharmacology and molecular docking analyses identified the MAPK and HIF-1α-signaling pathways as key therapeutic targets. In ISO-induced HCM mice, HYQT significantly improved cardiac morphology and function, reduced hypertrophic markers (ANP and BNP), inhibited myocardial collagen deposition, attenuated fibrosis, restored microvascular perfusion and density, and suppressed oxidative stress (MDA and ROS) and pro-inflammatory cytokine expression (TNF-α and IL-6). Mechanistically, in vitro experiments supported a cell-type-resolved, parallel regulatory effect: in HCMECs, HYQT-containing serum enhanced migration and viability, reduced ROS accumulation, and activated HIF-1α/VEGF-mediated angiogenic signaling, thereby alleviating microvascular dysfunction; concurrently, in H9C2 cardiomyocytes, HYQT inhibited phosphorylation of ERK, p38, and JNK, restored mitochondrial membrane potential, and reduced cell death, thereby mitigating hypertrophic remodeling and its downstream fibrotic progression.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;HYQT effectively ameliorates key pathological features of HCM, including myocardial hypertrophy, fibr","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/PMC13220444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053074","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":"Exploring the role of RCEO in macrophage-mediated modulation of pulmonary fibrosis.","authors":"Zhiguo Mao, Xiangke Lin, Xingyi Yang, Ying Liu, Chengfu Han, Shuo Tian, Yagang Song, Hui Zhao, Mingsan Miao","doi":"10.1186/s13020-026-01398-w","DOIUrl":"10.1186/s13020-026-01398-w","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Pulmonary fibrosis (PF) is an interstitial lung disease with macrophage polarization playing a critical role. Previous research has demonstrated that essential oil from Radix Curcumae (RCEO) significantly ameliorates pulmonary sarcoidosis, an effect attributed to the modulation of macrophage polarization. However, the therapeutic potential of RCEO in PF and its underlying mechanisms remain to be elucidated.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Purpose: &lt;/strong&gt;To investigate whether RCEO ameliorates pulmonary function in PF mice by suppressing the polarization of M1 and M2 macrophages via suppressing the Pi3k/Akt/β-catenin and Tlr4/Myd88/Nf-κb signaling pathways.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Bioinformatics and network pharmacology approaches were employed to predict the potential therapeutic targets of RCEO for PF. The main components of RCEO and the primary constituents of RCEO deposited in lung tissue following inhalation were analyzed using GC-MS. PF models were established both in vivo and in vitro using bleomycin. Changes in pulmonary function were assessed by whole-body plethysmography. HE staining and Masson staining were used to observe histopathological alterations and fibrosis progression in lung tissues. ELISA was performed to measure changes in fibrosis-related mediators in blood. Flow cytometry was utilized to investigate macrophage polarization and apoptosis levels in lung tissues. Immunofluorescence analysis was applied to quantify the expression and distribution of Tlr4 and Pi3k, as well as their fluorescence co-localization with macrophages, in lung tissues. PCR and WB were conducted to evaluate changes in mRNA expression levels and protein abundance associated with the Tlr4/Myd88/Nf-κb and Pi3k/Akt/β-catenin signaling pathways in lung tissues.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Bioinformatics and Network Pharmacology analyses predicted that the therapeutic effect of RCEO on PF is associated with the modulation of macrophage differentiation via the Tlr4/Myd88/Nf-κb pathway and the Pi3k/Akt/β-catenin signaling pathway. In a PF mouse model, RCEO significantly alleviated pathological alterations and collagen deposition in lung tissues and improved pulmonary function. Results from both in vivo and in vitro flow cytometry demonstrated that RCEO concurrently suppressed the differentiation of macrophages into both M1 and M2 phenotypes, promoted apoptosis in 3T3 cells while inhibiting apoptosis in MLE-12 cells, and reduced the levels of profibrotic mediators. Further PCR and Western blot analyses indicated that RCEO modulates macrophage polarization and extracellular matrix expression by inhibiting the Tlr4/Myd88/Nf-κb and Pi3k/Akt/β-catenin signaling pathways. Immunofluorescence assays revealed that RCEO effectively downregulated the expression of Tlr4 and Pi3k in macrophages, thereby exerting a protective effect against pulmonary fibrosis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;RCEO ameliorates PF by suppressing both M1 and M2 po","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/PMC13220479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053072","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}