Chinese Medicine最新文献

{"title":"Integrating multi-omics and machine learning strategies to explore the \"gene-protein-metabolite\" network in ischemic heart failure with Qi deficiency and blood stasis syndrome.","authors":"Jingjing Wei, Aolong Wang, Peng Yu, Yang Sun, Wenjun Wu, Yilin Zhang, Rui Yu, Bin Li, Mingjun Zhu","doi":"10.1186/s13020-025-01151-9","DOIUrl":"https://doi.org/10.1186/s13020-025-01151-9","url":null,"abstract":"<p><strong>Background: </strong>Ischemic heart failure (IHF) is a multifaceted syndrome associated with significant mortality and high hospitalization rates globally. According to traditional Chinese medicine (TCM) theory, Qi Deficiency and Blood Stasis (QXXY) Syndrome serves as the pathological basis of IHF. This study aims to investigate the biological basis of QXXY syndrome in IHF patients through an integrated multi-omics approach.</p><p><strong>Methods: </strong>We enrolled 100 participants, comprising 40 IHF patients with QXXY syndrome (IHF-QXXY), 40 IHF patients without QXXY syndrome, and 20 healthy controls. Utilizing an integrated approach combining RNA sequencing (RNA-seq), data-independent acquisition (DIA) proteomics, and targeted metabolomics, we established a comprehensive \"gene-protein-metabolite\" network for IHF-QXXY syndrome. Candidate biomarkers were identified through machine learning algorithms and further validated using RT-qPCR and targeted proteomics via intelligent parallel reaction monitoring (iPRM).</p><p><strong>Results: </strong>Patients with IHF-QXXY syndrome present with pronounced disruptions in energy metabolism, chronic inflammation, and coagulation abnormalities. The \"gene-protein-metabolite\" network of IHF-QXXY syndrome comprises six mRNAs, four proteins, and five metabolites. Key pathways involve the activation of neutrophil extracellular traps formation, platelet activation, the HIF-1 signaling pathway, and glycolysis/gluconeogenesis, alongside the suppression of the citrate cycle and oxidative phosphorylation. The key metabolites potentially associated with QXXY syndrome include 3-methylpentanoic acid, arachidonic acid, N-acetylaspartylglutamic acid, L-acetylcarnitine, and 12-hydroxystearic acid. We identified a panel of candidate biomarkers, including HIF-1α, IL10, PAD4, ACTG1, SOD2, GAPDH, FGA, FN1, F13A1, and ATP5PF. This biomarker combination significantly enhanced the diagnostic performance of IHF-QXXY syndrome (AUC > 0.863) and retained high diagnostic accuracy during validation (AUC > 0.75).</p><p><strong>Conclusion: </strong>This study provides a comprehensive characterization of the molecular features of QXXY syndrome in IHF patients, highlighting key pathways and biomarkers linked to energy metabolism dysregulation, chronic inflammation, and coagulation abnormalities. These findings may provide novel insights and methods for further advancing this research field.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"93"},"PeriodicalIF":5.3,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of mitochondria in the pharmacological and toxicological effects of Tripterygium wilfordii Hook F: functions, targets and new therapeutic applications.","authors":"Zhonghao Liu, Dan Li, Xiongwen Yang, Xisha Chen, Chengxiao Fu","doi":"10.1186/s13020-025-01170-6","DOIUrl":"https://doi.org/10.1186/s13020-025-01170-6","url":null,"abstract":"<p><p>Tripterygium wilfordii Hook F (TWHF) is a traditional Chinese medicine with multifaceted pharmacological properties, has faced clinical application challenges due to its dose-limiting organ toxicity. Through a systematic analysis of current literature, this review deciphers the dual regulatory role of mitochondrial function in mediating both therapeutic efficacy and adverse effects of TWHF-derived active compounds. We elucidate that processes such as mitochondrial biogenesis, mitochondrial fusion and fission, mitophagy and mitochondrial apoptosis pathways influence the therapeutic efficacy and adverse effects of TWHF active ingredients. In addition, we review innovative dosage forms and derivatives of TWHF that exploit mitochondrial targeting to enhance their pharmacological efficacy. This article offers a concise overview pharmacological and toxicological effects of the principal active components of TWHF, in particular triptolide and celastrol, with a particular emphasis on elucidating the critical role of mitochondria in these processes. Further high-quality basic studies are essential to strengthen the link between mitochondrial function and the active compounds of TWHF, offering more diverse options for their clinical development.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"114"},"PeriodicalIF":5.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aster tataricus extract and its active compounds display a broad spectrum of antiviral activity in vitro and in vivo.","authors":"Nuwan Gamage, Ji-Won Cha, Ji-Soo Jeong, Yebin Seong, Kiramage Chathuranga, Asela Weerawardhana, Jin Yeul Ma, Tae-Won Kim, Jong-Soo Lee","doi":"10.1186/s13020-025-01167-1","DOIUrl":"https://doi.org/10.1186/s13020-025-01167-1","url":null,"abstract":"<p><strong>Background: </strong>Aster tataricus, a perennial terrestrial herb with a rich history of use in traditional medicine, is renowned for its therapeutic properties. However, despite the widespread use of Aster tataricus, its antiviral efficacy and mode of action against viruses have not yet been studied. Here, we demonstrated that Aster tataricus extract (ATE) has antiviral effects and an underlying mechanism of action both in vitro and in vivo.</p><p><strong>Methods: </strong>Antiviral effect of ATE was assessed against Influenza A virus (PR8), Newcastle Disease Virus (NDV), and Herpes Simplex Virus-1 (HSV) in RAW264.7 cells. Mechanism was explored by analyzing the induction of antiviral immune responses, including type-I interferon (IFN) signaling and cytokine secretion. In vivo, BALB/c mice were treated with ATE prior to infection with lethal influenza A subtypes, A/PR/8/34 (H1N1), A/Aquatic bird/Korea/W81/2005 (H5N2), and A/Chicken/Korea/116/2004 (H9N2). Survival rates, viral titers, and lung pathology were measured. High-performance liquid chromatography (HPLC) was used to identify active compounds in ATE, and their antiviral effects were further investigated.</p><p><strong>Results: </strong>An effective dose of ATE significantly inhibited influenza A virus (PR8), NDV, and HSV replication in RAW264.7 cells. Mechanistically, we found that ATE induced an antiviral state, which includes upregulation of type-I interferon signaling and secretion of IFNs and pro-inflammatory cytokines in RAW264.7 cells. In vivo, ATE treatment showed increased survival due to reduced viral titers and less severe pathological changes in the lung, and the observed prophylactic effects were associated with increased secretion of IL-6, IFN-γ, and IFN-β in bronchoalveolar lavage fluid. Based on the reported information and HPLC analysis, quercetin, kaempferol, and ferulic acid were identified as active compounds in the aqueous fraction, and an effective dose of each compound exhibited antiviral effects similar to ATE against influenza viruses.</p><p><strong>Conclusions: </strong>These findings suggest that ATE and its active compounds act as immunomodulators and may be potential candidates as a source of promising natural antivirals for animals and humans.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"113"},"PeriodicalIF":5.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acupuncture promotes muscle cells ATP metabolism in ST36 acupoint local exerting effect by activating TRPV1/CaMKII/AMPK/PGC1α signaling pathway.","authors":"Zhihan Chen, Kaifang Yao, Xinrui Wang, Yangyang Liu, Simin Du, Shenjun Wang, Yuxin Fang, Yuan Xu, Zhifang Xu, Xiaowei Lin, Yi Guo","doi":"10.1186/s13020-025-01169-z","DOIUrl":"10.1186/s13020-025-01169-z","url":null,"abstract":"<p><p>At present, a number of studies have shown that acupuncture at Zusanli (ST 36) can relieve pain, but the changes of local microenvironment in the acupoint area after acupuncture have not been elucidated. As a temperature and pain receptor, TRPV1 plays an important role in pain perception and inflammation regulation. In this study, RT-PCR technique was used to screen the types of mechanically sensitive ion channels in the local response to acupuncture in the acupoint area, and western bolt technique was used to verify in gene knockout and antagonist injection mice. Immunofluorescence double labeling technique was used to further determine the key cell types of TRPV1-mediated acupuncture analgesia. Finally, through the combined analysis of proteomics and phosphorylated proteomics, the local signaling pathways of acupoints that can be activated by acupuncture were analyzed. This study systematically explored the analgesic effect of acupuncture on inflammatory pain in mice and its mechanism. The study found that acupuncture can significantly improve the thermal pain threshold and mechanical pain threshold in mice, showing a significant analgesic effect. Further analysis revealed that this analgesic effect was closely related to the up-regulation of local TRPV1 expression at ST36, and its deletion or functional inhibition would significantly weaken the analgesic effect of acupuncture. In addition, we also found that acupuncture in the deep muscle layer can more effectively promote the expression and activity of TRPV1 than in the superficial fascia layer, and muscle cells are the key cell types of TRPV1-mediated acupuncture analgesia. Finally, through the combined analysis of multi-omics, it was clear that acupuncture could activate the local signal pathway TRPV1/CaMKII/AMPK/PGC1α to exert analgesic effect. In conclusion, this study not only confirmed the analgesic effect of acupuncture on inflammatory pain in mice, but also revealed the core role of TRPV1 in the mechanism of acupuncture analgesia, especially the important contribution of TRPV1 expression and activity in the muscle layer of ST36 acupoint to the analgesic effect of acupuncture, which provided a new scientific basis and potential therapeutic target for acupuncture treatment of inflammatory pain.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"112"},"PeriodicalIF":5.3,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12257683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ganoderma lucidum spore oil alleviates psychological stress-evoked tumor progression by enhancing FcγR-mediated macrophage phagocytosis.","authors":"Dong-Dong Li, Zi-Xuan Li, Yang-Fan Zhou, Ling Jin, Wan-Li Liang, Wen-Dong Xu, Xiang Luo, Guan-Di Xiao, Qi-Jun Chen, Ting Xie, Hui Xu, Yang Liu, Hong-Fei Cai, Yun-Feng Cao, Wan-Yang Sun, Yi-Fang Li, Lei Liang, Ju-Yan Liu, Yan-Ping Wu, Rong-Rong He","doi":"10.1186/s13020-025-01168-0","DOIUrl":"10.1186/s13020-025-01168-0","url":null,"abstract":"<p><strong>Background: </strong>Ganoderma lucidum (G. lucidum), has been documented as a medicinal herb in classical texts and officially recognized in both Eastern and Western pharmacopeias. G. lucidum spore oil (GLSO), a lipid substance extracted from sporoderm-broken spores, has shown potential in enhancing immune function and prolonging the survival of tumor patients. However, the mechanisms underlying GLSO's immunomodulatory effects remain poorly unknown.</p><p><strong>Methods: </strong>The effect of psychological stress on tumor progression and macrophage phagocytosis was analyzed by an in vivo small animal imaging system and flow cytometry. The effect of psychological stress on phospholipid composition in mice was investigated by LC-MS/MS based lipidomic analysis. The effectiveness of GLSO in tumor-bearing mice subjected to restraint stress was observed by tumor burden and phagocytosis of macrophages. Finally, the underlying mechanism of GLSO on macrophage phagocytosis in mice subjected to psychological stress was explored by RNA-seq, and the FcγR/SYK-mediated macrophage phagocytosis pathway was confirmed by qPCR, Western blotting, and confocal laser technology.</p><p><strong>Results: </strong>Our study discovered that psychological stress-triggered tumor progression is contributed to by liposoluble components-impaired macrophage phagocytosis. Lipidomics analysis further identified lysophosphatidylinositol [LPI (18:0)] as a key factor suppressing macrophage phagocytic capacity under psychological stress. GLSO was shown to mitigate psychological stress-evoked tumor progression by enhancing macrophage-mediated phagocytosis of tumor cells in vivo. Mechanistically, transcriptomics analysis revealed that the LPI-mediated FcγR phagocytosis pathway is a crucial axis driving the therapeutic effect of GLSO under psychological stress.</p><p><strong>Conclusion: </strong>Our findings illustrate that psychological stress-promoted cancer progression is contributed by the critical liposoluble components LPI (18:0)-mediated FcγR phagocytosis signaling inhibition. GLSO alleviates the dampened phagocytosis of macrophages caused by stress through regulating LPI/FcγR-mediated phagocytosis-related pathways, underscoring its potential as a therapeutic intervention for stress-related tumor progression.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"111"},"PeriodicalIF":5.3,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12257750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636336","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":"Effects of solamargine in hepatic metastasis of colorectal cancer: induction of ferroptosis and elimination of cancer stem cells.","authors":"Shenglan Liu, Junhong Wu, Hao Huang, Bin Hu, Dong Xie, Fuqiang Cao, Jingxuan Li, Caiyao Guo, WeiJie Peng, Yanli Jin, Wei Dai","doi":"10.1186/s13020-025-01171-5","DOIUrl":"10.1186/s13020-025-01171-5","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is a prevalent malignant tumor globally, ranking third in incidence and second in mortality. Metastasis is the main cause of death in patients with CRC. Solanum nigrum L. (SNL), a traditional Chinese medicinal herb endowed with detoxification, blood circulation enhancement, and anti-swelling properties, has been widely used in folk prescriptions for cancer treatment in China. Solamargine (SM) is the major steroidal alkaloid glycoside purified from SNL. However, its role and mechanism against metastatic CRC are not yet clear. The purpose of this study was to evaluate the inhibitory effect of SM on human hepatic metastatic CRC and investigate its underlying mechanism.</p><p><strong>Methods: </strong>CCK-8 assay, colony-formation assay, transwell assay, flow cytometry, tumoursphere formation assay, reverse-transcription quantitative PCR (RT-qPCR), Western blotting, transcriptomic sequencing and ferroptosis analysis were performed to reveal the efficacy and the underlying mechanism of SM in CRC cell lines. In vivo, allograft model, patient-derived xenograft (PDX) model, and liver metastatic model were performed to verify the effect of SM on the growth and metastasis of CRC.</p><p><strong>Results: </strong>SM was found to suppress hepatic metastasis in CRC by effectively targeting key cellular processes, including proliferation, survival, and stemness. RNA sequencing showed that SM could induce ferroptosis, which was confirmed by elevated lipid reactive oxygen species (ROS) and downregulated glutathione peroxidase 4 (GPX4) and glutathione synthetase (GSS) in CRC cells and xenografts. Induction of ferroptosis by SM was regulated by nuclear factor erythroid 2-related factor 2 (Nrf2). Furthermore, downregulation of β-catenin was found to be fundamental for the SM-enabled cancer stem cells (CSCs) elimination and metastasis blockage in CRC.</p><p><strong>Conclusion: </strong>Our results indicated that SM is a promising therapeutic drug to inhibit hepatic metastasis in CRC by inducing ferroptosis and impeding CSCs.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"110"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616570","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":"Juanbi Qianggu Formula inhibits fibroblast-like synovicytes activation via repressing LncRNA ITSN1-2 to promote RIP2 K48 ubiquitination.","authors":"Yanqin Bian, Fang Li, Xinyu A, Zheng Xiang, Nanshan Ma, Jianye Wang, Boran Cao, Pengfei Xin, Xuan Cheng, Chang Liu, Bei Xiang, Jun Shen, Qigui Lu, Lianbo Xiao","doi":"10.1186/s13020-025-01164-4","DOIUrl":"10.1186/s13020-025-01164-4","url":null,"abstract":"<p><strong>Background: </strong>Long non-coding RNA ITSN1-2(lncRNA ITSN1-2) promotes fibroblast-like synovicytes (FLS) proliferation and suppress apoptosis through activation of the NOD2/RIP2 signaling pathway, thereby exacerbating synovitis in Rheumatoid arthritis (RA) pathology. Juanbi Qianggu Formula (JBQG), a clinically efficacious traditional Chinese medicine, has shown significant efficiency in inhibiting FLS activation in RA and alleviating disease progression in RA patients. However, the molecular mechanism underlying JBQG's anti-arthritic effects remains incompletely understood, particularly regarding its potential to modulate lncRNA ITSN1-2-mediated NOD2/RIP2 signaling in FLS activation. This study aims to investigate the functional interplay between JBQG and the lncRNA ITSN1-2/NOD2/RIP2 axis in regulating FLS behavior during RA development.</p><p><strong>Methods: </strong>Synovial tissues were collected from 24 rheumatoid arthritis (RA) patients and 20 osteoarthritis (OA) patients to observe the lncRNA ITSN1-2/NOD2/RIP2 signal in RA synovial tissue and its correlation with RA inflammation and bone destruction. Blood-absorbed components of JBQG were analyzed through mass spectrometry, while network pharmacology and in vitro experiments were conducted to investigate JBQG's regulatory effects on NOD2/RIP2 signaling. Mechanistic studies focused on lncRNA-ITSN1-2/miR-2683-3p/PELI3/RIP2 interactions, employing dual-luciferase assays, FISH staining, and Co-IP/Western blot. To evaluate therapeutic efficacy, a collagen-induced arthritis (CIA) rat model with lncRNA ITSN1-2 overexpression was established. JBQG's effects were assessed through histopathological examination and serum inflammation factors analysis following 23 g/kg/day treatment for 4 weeks.</p><p><strong>Results: </strong>LncRNA ITSN1-2/NOD2/RIP2 signaling was significantly activated in RA synovial tissues, showing profound correlation with RA disease inflammation and progression. JBQG treatment reduced cytoplasmic lncRNA ITSN1-2 levels in FLS, thereby inhibiting NOD2/RIP2 pathway activation and FLS functions in migration and invasion. Mechanistically, lncRNA ITSN1-2 exerted competitive endogenous RNA (ceRNA) activity by sequestering miR-2683-3p, which upregulated PELI3 expression. This induction promoted RIP2 K48 ubiquitination, destabilizing RIP2 protein integrity and inhibiting downstream NF-κB signaling. Consequently, FLS migratory and invasive capacities were significantly diminished, underscoring JBQG's dual regulatory impact on lncRNA-miRNA cross-talk and inflammatory cytokine cascades.</p><p><strong>Conclusion: </strong>This study demonstrates that JBQG exerts potent anti-arthritic effects in RA therapy through dual regulatory mechanisms targeting the lncRNA ITSN1-2/miR-2683-3p/PELI3/RIP2 axis.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"109"},"PeriodicalIF":5.3,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590588","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":"Buyang Huanwu Decoction improves energy metabolism disorders after cerebral ischemia-reperfusion by regulating the SIRT1/AMPK signaling pathway to promote glycolysis and the tricarboxylic acid cycle.","authors":"Zhongji Hu, Nujiao Deng, Yanling Li, Yang Bai, Xiao Lan, Tingting Xiong, Huang Ding, Xiaodan Liu, Changqing Deng","doi":"10.1186/s13020-025-01163-5","DOIUrl":"10.1186/s13020-025-01163-5","url":null,"abstract":"<p><strong>Background: </strong>Buyang Huanwu Decoction (BYHWD), a traditional Chinese medicine formula for cerebral infarction, exerts neuroprotective effects by enhancing cerebral energy metabolism, yet its precise mechanisms remain elusive.</p><p><strong>Objective: </strong>To explore the effects of BYHWD on improving cerebral ischemia-reperfusion injury (CIRI) with Qi deficiency and blood stasis syndrome from an energy metabolism perspective and verify it through experiments.</p><p><strong>Methods: </strong>A rat model of CIRI with Qi deficiency and blood stasis syndrome was established and intervened with BYHWD. The therapeutic effect of BYHWD was evaluated using Longa score, Qi deficiency and blood stasis syndrome score, pathological staining, and colorimetric assays. Untargeted metabolomics was used to identify differential metabolites and regulatory mechanisms, and in vivo and in vitro models were constructed for validation.</p><p><strong>Results: </strong>BYHWD ameliorated neurological deficits and Qi deficiency and blood stasis syndrome in rats, reduced brain pathology, and increased energy substances. Untargeted metabolomics analysis suggested BYHWD enhanced cerebral energy metabolism via nicotinate and nicotinamide metabolism and AMPK signaling, involving SIRT1/AMPK regulation and promotion of glycolysis and the tricarboxylic acid (TCA) cycle. Validation experiments showed BYHWD activated the SIRT1/AMPK signaling pathway in brain tissue, promoting glucose uptake and enhancing the expression of proteins related to glycolysis, mitochondrial biogenesis, and the TCA cycle. Similar results were observed in HT22 cells subjected to oxygen-glucose deprivation/reperfusion (OGD/R).</p><p><strong>Conclusion: </strong>BYHWD improved cerebral energy metabolic disorders by activating the SIRT1/AMPK signaling pathway, thereby enhancing glycolytic capacity and TCA cycle capacity. This study elucidated the mechanisms of BYHWD and provided a theoretical basis for its rational application.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"108"},"PeriodicalIF":5.3,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12232815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583232","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":"Herb-drug interactions in oncology: pharmacodynamic/pharmacokinetic mechanisms and risk prediction.","authors":"Xiaoyan Duan, Xiaoyu Fan, Haiyan Jiang, Jie Li, Xue Shen, Zeao Xu, Ziqi Zhou, Jia Xu, Chongze Chen, Hongtao Jin","doi":"10.1186/s13020-025-01156-4","DOIUrl":"10.1186/s13020-025-01156-4","url":null,"abstract":"<p><p>The prevalence of herbal medicines has gained widespread, particularly among cancer patients seeking adjunctive therapies. Co-administered with anticancer drugs (ACDs) frequently, herbal medicines result in increasing cases of herb-drug interactions (HDIs), following the serious clinical consequences. While herbal medicines pose negative impacts, such as limiting efficacy and increasing toxicity of ACDs, they also offer potential benefits, including enhancing bioavailability, reducing adverse reactions, and reversing tumor drug resistance. This review is the first to systematically characterize HDI molecular mechanisms at both pharmacodynamic (PD) and pharmacokinetic (PK) levels, elucidating how herbal medicines modulate ACDs efficacy and safety through antagonism/synergy/detoxification target, metabolic enzymes, and transporters. In particular, emerging risk prediction methodologies are proposed to assess the clinical occurrence of potential PD/PK-mediated HDIs. We provide a novel insight for promoting the mechanism study of HDIs, facilitating the safe and effective integration of herbal medicines into cancer treatment.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"107"},"PeriodicalIF":5.3,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12232703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583233","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":"Integration bile acid metabolomics and gut microbiome to study the anti-liver fibrosis effects of total alkaloids of Corydalis saxicola Bunting.","authors":"Qianyi Wang, MeiLing Zhang, Mingwei Meng, Zhuo Luo, Ziping Pan, Lijun Deng, Jinghua Qin, Bingjian Guo, Dan Zhu, Yanmin Zhang, Hongwei Guo, Yonghong Liang, Zhiheng Su","doi":"10.1186/s13020-025-01158-2","DOIUrl":"10.1186/s13020-025-01158-2","url":null,"abstract":"<p><strong>Background: </strong>Bile acids and gut microbiota participate in the pathogenesis of liver fibrosis (LF). The total alkaloids of Corydalis saxicola Bunting (TACS) is a traditional Chinese medicine extract that has been used to treat LF, but the underlying mechanisms are not clear. This study performed integrated metabolomics and gut microbiome analysis to study the anti-LF mechanism of TACS using a rat model.</p><p><strong>Methods: </strong>Ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) was used to identify the chemical compounds in TACS. Biochemical and histopathological analysis were performed to determine the efficacy of TACS. Bile acid-targeted metabolomics was used to assess changes in the bile acid (BA) profiles in TACS-treated LF rats. 16S rRNA gene sequencing and metagenomics were used to assess changes in the gut microbiota of the TACS-treated LF rats. Antibiotic cocktail treatment and fecal microbiota transplantation (FMT) were used to determine the relationship between the gut microbiota and the anti-LF effects of TACS. Metagenomics was used to identify significantly enriched gut microbiota after TACS treatment and its correlation with the anti-LF effects was verified by in vivo experiments.</p><p><strong>Results: </strong>TACS treatment significantly reduced the levels of serum liver enzymes, fibrosis and pro-inflammatory cytokines in the liver. TACS significantly increased the levels of chenodeoxycholic acid (CDCA) and taurochenodeoxycholic acid (TCDCA) in the cecum and decreased the levels of cholic acid (CA) and deoxycholic acid (DCA) in the liver of the LF rats. TACS significantly increased the abundances of Lactobacillus and Akkermansia in the LF rats. Antibiotic cocktail treatment and FMT have shown that the effect of TACS cure liver fibrosis depends on the gut microbiota. The abundance of Lactobacillus reuteri was significantly increased by TACS. Administration of Lactobacillus reuteri via gavage ameliorated LF.</p><p><strong>Conclusions: </strong>TACS exerted anti-LF effects in rats by modulating bile acid metabolism and gut microbiome.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"106"},"PeriodicalIF":5.3,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559387","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}