Chinese Medicine最新文献

{"title":"Sodium tanshinone IIA sulfonate alleviates osteoarthritis through targeting SIRT1.","authors":"Mao Xu, Xulei Sun, Xiao Ma, Zixuan Qin, Xin Gao, Xinxin Jin, Hongzhi Sun","doi":"10.1186/s13020-025-01166-2","DOIUrl":"10.1186/s13020-025-01166-2","url":null,"abstract":"<p><strong>Background: </strong>Osteoarthritis (OA), a chronic degenerative disease, is characterized by the loss of articular cartilage, impacting more than 500 million individuals worldwide. Sodium tanshinone IIA sulfonate (STS) is a water-soluble derivative of tanshinone IIA derived from Salvia miltiorrhiza and has anti-inflammatory and anti-oxidative functions. Although STS shows significant pharmacological effects and mechanisms in treating various diseases in vivo and in vitro, its specific treatments and mechanisms for OA remain largely unknown.</p><p><strong>Materials and methods: </strong>Primary chondrocytes were stimulated with interleukin-1β (IL-1β) to establish an in vitro OA model. The optimal concentration of STS for application on chondrocytes was determined to be 100 μM using MTT assays. The effects of STS on catabolic gene expression were assessed through real-time quantitative PCR (RT-qPCR). Western blotting, immunoprecipitation (IP), and mutation techniques were employed to investigate the impact of STS on the deacetylation of nuclear factor kappa B subunit p65 (NF-κB p65) at Lys310 by silent information regulator 1 (SIRT1). Furthermore, RT-qPCR, Enzyme-linked immunosorbent assay (ELISA), transmission electron microscopy, and immunohistochemistry staining were utilized to elucidate the molecular mechanisms underlying NF-κB-driven inflammation and ferroptosis. The destabilization of the medial meniscus (DMM) surgery-induced OA mouse model was employed to evaluate the therapeutic potential of STS in OA treatment. Safranin O-fast green and hematoxylin and eosin (HE) staining analyses were conducted to assess the impact of STS on OA. Additionally, tamoxifen (TM)-inducible Sirt1 cartilage-specific conditional knockout (Sirt1cKO) mice were utilized to further validate the effects of STS on OA.</p><p><strong>Results: </strong>STS suppressed the gene expression levels of collagen type X alpha 1 (COL10A1), matrix metalloproteinase-13 (MMP13), and Caspase3, thereby mitigating matrix degradation and apoptosis in IL-1β-induced primary chondrocytes. Additionally, STS enhanced the expression of SIRT1 in these cells. Furthermore, STS facilitated the deacetylation of NF-κB p65 at Lysine (K) 310 by SIRT1 in primary chondrocytes. STS also inhibited NF-κB p65-mediated inflammation and ferroptosis, contributing to the amelioration of OA. In the DMM surgery-induced OA mice model, STS mitigated OA phenotypes by inhibiting matrix degradation and apoptosis, facilitating SIRT1-mediated deacetylation of NF-κB p65, and subsequently suppressing NF-κB p65-driven inflammation and ferroptosis. Finally, the use of Sirt1cKO transgenic mice further confirmed the effects of STS in attenuating OA progression.</p><p><strong>Conclusion: </strong>STS ameliorated OA by activating SIRT1 and inhibiting NF-κB p65-driven inflammation and ferroptosis, indicating its potential therapeutic application in OA patients.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"142"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944945","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 potential bioactive compounds group and mechanism of Ci Bai Capsule in treating leukopenia: a combined approach of network pharmacology and transcriptome evidences.","authors":"Dingfan Zhang, Congshu Huang, Lei Zhou, Boyang Wang, Wei Zhou, Tiantian Xia, Pan Shen, Shao Li, Yue Gao","doi":"10.1186/s13020-025-01197-9","DOIUrl":"10.1186/s13020-025-01197-9","url":null,"abstract":"<p><strong>Background: </strong>Radiation-induced leukopenia caused by low-dose exposure is frequently associated with Traditional Chinese Medicine (TCM) syndromes like \"blood deficiency\" and \"fatigue syndrome\". Ci Bai Capsule (CB) has been reported to enhance white blood cell levels; however, its mechanisms and bioactive compounds remain unclear.</p><p><strong>Aim: </strong>This study aimed to identify the bioactive compounds group of CB and elucidate its potential mechanisms in radiation-induced leukopenia.</p><p><strong>Methods: </strong>Syndrome-related data were gathered from SYMMAP and CTD database. CB's target profile is predicted by DrugCIPHER. Network pharmacology approaches were employed to identify active compounds and related pathways. Experimental validation was conducted through flow cytometry, RNA-sequencing both ex vivo and in vivo models. RT-qPCR and Western blot were performed for quantitative validation of key targets.</p><p><strong>Results: </strong>A total of 22 pathways related to cellular processes, immune responses, and signal transduction were identified. Five key bioactive compounds (kaempferol-3-glucorhamnoside, syringin, schisandrin, 3-hydroxytyrosol 3-O-glucoside and salidroside) were found to significantly modulate syndrome-related pathways. Optimal dosing of this compound combination enhanced leukocyte counts and splenic immune cell proliferation in irradiated mice. Transcriptomic analysis revealed that the compounds exert regulatory effects on PP1A, RB, CDK4/6, CDK2, and CDK1, thereby modulating downstream immune and hematopoietic markers such as MNDA, BST2, and HSPA1A.</p><p><strong>Conclusion: </strong>Our findings suggest that CB mitigates radiation-induced leukopenia by enhancing immune and hematopoietic recovery, offering a promising therapeutic approach for managing radiation-related hematological disorders.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"139"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400580/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945085","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":"Potential of phytochemicals in the treatment of Alzheimer disease by modulating lysosomal dysfunction: a systematic review.","authors":"Man Yuan, Trinh Thach Thi Nguyen, Alasdair J Gibb, Yan-Fang Xian, Hong-Xi Xu","doi":"10.1186/s13020-025-01204-z","DOIUrl":"10.1186/s13020-025-01204-z","url":null,"abstract":"<p><p>Alzheimer disease (AD) is a primary international health dilemma, especially in elderly populations, due to its progressive nature and its adverse cognitive impact. The dysfunction of lysosomes, which impairs protein degradation and leads to toxic accumulation in neurons, is a pivotal factor in AD. We explore phytochemicals that specifically target lysosomal dysfunction via the activation of autophagy, phagocytosis, and lysosome function, exhibiting anti-inflammatory and antioxidant properties. This study involves extracting and evaluating phytochemicals by exploring multiple databases, Google Scholar, PubMed, the Science Citation Index Expanded (SCIE), and the China National Knowledge Infrastructure (CNKI), integrating contemporary biochemical evidence with TCM principles-highlighting the interconnected roles of deficiency, stasis, and phlegm-to provide a comprehensive therapeutic framework. Key phytochemicals-magnolol, trehalose, and salidroside- demonstrate notable promise in enhancing lysosomal function, reducing amyloid beta accumulation, and improving cognitive outcomes. Addressing traditional theory and modern science, we underline the potential for future research by clarifying the mechanisms of compounds and their effectiveness, which may delay the disease process.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"138"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944971","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":"Integrated metabolomics and the microbiome reveal the compatibility mechanism of the Suxiao Jiuxin pill in the treatment of stable coronary artery disease.","authors":"Wanqi Le, Jingyu Liao, Yuhao Zhang, Jingjing Xu, Yuanyuan Zeng, Houkai Li, Xiaoxu Shen, Gaosong Wu, Weidong Zhang","doi":"10.1186/s13020-025-01198-8","DOIUrl":"10.1186/s13020-025-01198-8","url":null,"abstract":"<p><strong>Background: </strong>The Suxiao Jiuxin pill (SJP) is a Chinese patent medicine that is used for the treatment of stable coronary artery disease (SCAD). However, the compatibility mechanism of SJP in treating of SCAD is still unclear. This study aimed to elucidate the serum metabolic profiles of patients with SCAD treated with SJP and to decipher the compatibility mechanism of its effective components, Chuanxiong Rhizoma and borneol.</p><p><strong>Methods: </strong>We employed metabolomics to assess the serum metabolic profiles of SCAD patients before and after treatment with SJP through metabolomics. Additionally, the compatibility mechanism of the multicomponent pairing of Chuanxiong Rhizoma and borneol was explored using metabolomics and 16S rRNA sequencing.</p><p><strong>Results: </strong>Our findings indicate that SJP significantly modulates lipid metabolism in SCAD patients, with particular impacts on glycerophospholipids and fatty acyls. Coadministration of Chuanxiong Rhizoma and borneol in mice demonstrated that borneol increases the absorption of the active components of Chuanxiong Rhizoma into the blood in a dose-dependent manner. This effect correlated with the dose-dependent enrichment of A. muciniphila and its role in modulating host lipid metabolism (glycerophospholipids and fatty acyls). Moreover, the combination of A. muciniphila and Chuanxiong Rhizoma also significantly promoted the absorption of the active components of Chuanxiong Rhizoma into the blood and affected host lipid metabolism (glycerophospholipids and fatty acyls).</p><p><strong>Conclusion: </strong>This study is the first to demonstrate a link between SJP treatment in SCAD patients and improved lipid metabolism. Borneol enriches A. muciniphila in a dose-dependent manner, thereby regulating host lipid metabolism and facilitating the absorption of the active components of Chuanxiong Rhizoma into the blood.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"140"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945096","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":"Houttuynia cordata Thunb-derived extracellular vesicle-like particles alleviate ischemic brain injury by miR159a targeting ACSL4 to suppress ferroptosis.","authors":"ShenYang Zhang, ZhiYan Liang, ChunYi Wu, ZiLu Qin, XueWen Wei, YiNing Liu, RuiQi Su, LiLi Li, Bin Sun, LinYan Huang, Wan Wang, JianGang Shen, GuangSheng Wang, SuHua Qi","doi":"10.1186/s13020-025-01193-z","DOIUrl":"10.1186/s13020-025-01193-z","url":null,"abstract":"<p><strong>Introduction: </strong>Neuroprotective agents for acute ischemic stroke often fall short in efficacy due to the blood-brain barrier challenges, lack of target specificity, and limited effectiveness. Recently, plant-derived extracellular vesicle-like particles (EVLP) have shown promise in their multifaceted functions.</p><p><strong>Objectives: </strong>The neuroprotective advantages that EVLP produced from Houttuynia cordata Thunb against cerebral ischemia/reperfusion injury are investigated.</p><p><strong>Methods: </strong>The extraction of HT-EVLP was performed using gradient centrifugation and ultracentrifugation, followed by identification of its particle size, morphology, and exosomal marker proteins. Using behavioral tests and a rat model of middle cerebral artery occlusion (MCAO), the neuroprotective attributes of HT-EVLP were assessed. To evaluate the effect of HT-EVLP on ferroptosis and cell survival, the oxygen-glucose deprivation/reoxygenation (OGD/R) induced HT22 cell model was used. Utilizing bioinformatics analysis and small RNA sequencing, the miRNA composition and downstream target genes of HT-EVLP were predicted. The dual-luciferase reporter gene assay was used to confirm that miR159a bound to long-chain acyl-coenzyme A synthase 4 (ACSL4). The impact of miR159a transfection on OGD/R-induced ferroptosis in HT22 cell was also observed.</p><p><strong>Results: </strong>Using a MCAO model, we found that HT-EVLP preserved blood brain barrier integrity, naturally penetrated the infarct core area, reduced cerebral infarct volume, mitigated neuronal apoptosis and ferroptosis, and facilitated recovery of neuronal function. In vitro studies further revealed that HT-EVLP enhanced cell survival and suppressed ACSL4-mediated ferroptosis in OGD/R-treated HT22 cells. Small RNA sequencing indicated that HT-EVLP are rich in miRNAs, with miR159a, among the top 10, potentially regulating ferroptosis-related pathways and directly binding to the 3'UTR of ACSL4. Overexpression of miR159a reduced Erastin-induced ACSL4 expression and alleviated mitochondrial damage in HT22 cells without causing toxicity.</p><p><strong>Conclusions: </strong>This study highlights the potential of HT-EVLP as carriers of endogenous miR159a, offering a promising strategy for ischemic brain injury therapy.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"141"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945121","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":"Maimendong decoction and its active ingredient, ophiopogonin D, alleviate bleomycin-induced pulmonary fibrosis by regulating the behavior of lung fibroblasts.","authors":"Mingjie Yang, Xinyue Zhang, Shengchuan Bao, Shusen Yang, Yilin Zhang, Yushan Liu, Chengjun Li, Junbo Zou, Jingtao Li, Shuguang Yan","doi":"10.1186/s13020-025-01206-x","DOIUrl":"10.1186/s13020-025-01206-x","url":null,"abstract":"<p><strong>Background: </strong>Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by progressive scarring of lung tissue, which can lead to respiratory failure and other serious complications, making the search for safe and effective therapeutic agents an urgent priority; Maimendong Decoction (MMDD), a traditional Chinese herbal formula widely employed in clinical practice to treat pulmonary disorders, has been shown to reduce inflammatory cytokines, suppress pro-fibrotic factors, and alleviate oxidative stress, yet the precise mechanisms by which MMDD exerts its anti-fibrotic effects remain unclear.</p><p><strong>Purpose: </strong>This study aims to evaluate the therapeutic efficacy of MMDD in pulmonary fibrosis and to elucidate its underlying mechanisms.</p><p><strong>Methods: </strong>Using a bleomycin (BLM)-induced mouse model of idiopathic pulmonary fibrosis, we assessed the therapeutic impact of MMDD on pulmonary fibrosis; concurrently, Ophiopogonin-D (OP-D), a principal active ingredient of MMDD, was evaluated in an in vitro human fetal lung fibroblast model treated with transforming growth factor-β (TGF-β) to elucidate its precise anti-fibrotic mechanism; finally, multi-omics technologies and bioinformatics analyses were employed for comprehensive validation.</p><p><strong>Results: </strong>MMDD ameliorated the degeneration observed in BLM-induced pulmonary fibrosis by curbing fibroblast activation and the over-deposition of extracellular matrix. Comprehensive multi-omics and bioinformatics analyses further indicated that MMDD modulates fibroblast behaviors-including proliferation and ferroptosis-through inhibition of the TGF-β signaling pathway. In vitro studies showed that OP-D induces ferroptosis in TGF-β-treated lung fibroblasts by blocking the negative regulatory signals of ferroptosis, mainly via downregulation of Ferritin Heavy Chain 1 (FTH1) expression. Moreover, overexpressing FTH1 nullified the anti-fibrotic activity of OP-D.</p><p><strong>Conclusion: </strong>The results of this study indicate that MMDD and its active component, OP-D, can treat IPF by targeting the proliferation of lung fibroblasts.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"135"},"PeriodicalIF":5.7,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944956","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":"Impact of Traditional Chinese Medicine therapy focused on strengthening the body on postoperative recurrence and metastasis prevention in stage IIIA non-small cell lung cancer: a real-world retrospective cohort study.","authors":"Ruoyan Qin, Yi Jiang, Liping Shen, Jie Qian, Yanlan Kang, Rui Fan, Lingshuang Liu","doi":"10.1186/s13020-025-01195-x","DOIUrl":"10.1186/s13020-025-01195-x","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to evaluate the impact of Traditional Chinese Medicine (TCM) therapy focused on strengthening the body on postoperative recurrence and metastasis prevention in patients with stage IIIA non-small cell lung cancer (NSCLC).</p><p><strong>Methods: </strong>This retrospective cohort study analyzed real-world data from patients with stage IIIA NSCLC who underwent radical surgery between January 2016 and January 2022 at Longhua Hospital, Shanghai University of Traditional Chinese Medicine. Patients were classified into an exposed group, receiving adjuvant chemotherapy or radiotherapy combined with TCM therapy, and a non-exposed group, receiving only adjuvant chemotherapy or radiotherapy. The primary outcome was disease-free survival (DFS), while secondary endpoints included 1-year, 2-year, and 3-year DFS rates (DFSR).</p><p><strong>Results: </strong>A total of 700 patients were included, with 340 in the exposed group and 360 in the non-exposed group. After propensity score matching, the exposed group demonstrated a significantly longer median DFS compared to the non-exposed group (32.0 months [95% CI 24.0-38.0] vs. 17.0 months [95% CI 15.0-20.0], p < 0.001) and higher 1-year, 2-year, and 3-year DFS rates (78% vs. 63%, 56% vs. 38%, and 44% vs. 24%, respectively; p < 0.001). TCM therapy was associated with reduced recurrence and metastasis (HR = 0.58, 95% CI 0.48-0.70, p < 0.001). Subgroup analysis showed greater DFS benefits following TCM therapy in patients with N2 involvement and those over 65 years (both p < 0.05).</p><p><strong>Conclusions: </strong>TCM therapy focused on strengthening the body may prolong DFS and improve DFSR in postoperative stage IIIA NSCLC patients. However, further large-scale prospective studies are needed to validate these findings.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"137"},"PeriodicalIF":5.7,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945082","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":"Sea cucumber polypeptide ameliorates aging properties via the brain-gut axis in naturally aging mice.","authors":"Chao Feng, Yiwen Shou, Shulin Wu, Han Mo, Xin Mao, Huisha Huang, Qinpei Lu, Li Xia, Lu Lu, Zhiheng Su, Hongwei Guo, Zhaoquan Huang","doi":"10.1186/s13020-025-01201-2","DOIUrl":"10.1186/s13020-025-01201-2","url":null,"abstract":"<p><strong>Background: </strong>Sea cucumber has been recognized as a traditional nutraceutical in Chinese medicine for millennia, with its derived polypeptide (SCP) demonstrating diverse bioactive properties. Nevertheless, the molecular mechanisms underlying SCP's potential geroprotective effects remain insufficiently characterized.</p><p><strong>Methods: </strong>We systematically evaluated SCP's impact on neuromotor function and cognitive performance in physiologically aged C57BL/6 J mice models using a behavioral test battery comprising open field, Y-maze, and Barnes maze paradigms. Complementary multi-omics approaches were employed to interrogate age-related perturbations in gut microbial ecology (16S rRNA sequencing) and systemic metabolism (untargeted LC-MS).H&E and immumohistochemical staining was used to evaluate the pathological features of mice brain tissues and intestinal tissue. Bulk RNA-sequencing was used to detect gene expression profiles in mice brain tissue.</p><p><strong>Results: </strong>Behavioral assessments (open field, Y-maze, Barnes maze) demonstrated that SCP intervention effectively delayed the decline in exercise, learning and memory abilities in aging mice. SCP administration enhanced cerebral organosomatic indices and hepatic functional markers while reducing neuronal senescence biomarkers. Furthermore, SCP improved intestinal mucosal barrier function in aging mice restored gut microbial diversity metrics, effectively counteracting age-associated dysbiosis. Mechanistically, SCP induced taxonomic restructuring characterized by increased abundance of neuroprotective Eubacterium_brachy_group and Prevotellaceae genera, concomitant with suppression of dementia-linked Dubosiella. Metabolomic integration revealed SCP-mediated upregulation of steroidogenic pathways correlating with cognitive enhancement. Multi-omics validation through integrated transcriptomic profiling and immunohistochemical quantification corroborated these physiological improvements.</p><p><strong>Conclusion: </strong>Our findings propose a mechanism whereby SCP might exert geroprotective effects through multimodal regulation of the gut-brain axis and systemic metabolic homeostasis, establishing mechanistic foundations for its translational potential in healthy longevity promotion.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"136"},"PeriodicalIF":5.7,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944942","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":"Yuye Jinhua Qingre Tablets Attenuate Acute Pharyngitis by inhibiting the Complement Cascade and C5a/C5aR1 Axis.","authors":"Yifei Gao, Leiming You, Jiying Zhou, Xiaoyu Tao, Zhengsen Jin, Chao Wu, Fanqin Zhang, Siyu Guo, Haojia Wang, Yueqin Guan, Hua Luo, Jiarui Wu","doi":"10.1186/s13020-025-01191-1","DOIUrl":"10.1186/s13020-025-01191-1","url":null,"abstract":"<p><strong>Background: </strong>Acute pharyngitis (AP) is a common upper respiratory tract infection, primarily characterized by symptoms such as throat pain, redness, swelling, and difficulty swallowing. It is typically caused by viral infections, bacterial infections, or physical and chemical irritants. Yuye Jinhua Qingre Tablets (YYJH) are recognized for their ability to clear heat, detoxify, reduce swelling, and alleviate pain, making them a common treatment option for acute pharyngitis. However, research on their specific mechanisms of action is still inadequate.</p><p><strong>Methods: </strong>Using UPLC-Q-Exactive-Orbitrap-MS technology combined with serum pharmacochemical analysis, the main chemical components and blood components of YYJH were identified. The anti-inflammatory activity was verified through the ammonia-induced acute pancreatitis (AP) model in SD rats and the LPS-stimulated NP69SV40T cell inflammation model. Integrating transcriptomics, proteomics, and bioinformatics analysis revealed the mechanism of YYJH in treating AP, which was further validated by molecular biology experiments.</p><p><strong>Results: </strong>Twelve blood-entry components were identified, and their anti-inflammatory effects were validated using the SD rat acute pancreatitis (AP) model and the NP69SV40T cell inflammation model. The study results indicated that the drug significantly improved the pathological damage of the pharyngeal mucosa in rats with the AP model, reducing the levels of inflammatory cells in peripheral blood and serum inflammatory factors. The combined analysis of transcriptomics and Astral DIA proteomics revealed that the anti-inflammatory effects of YYJH are associated with the regulation of the classical complement pathway, characterized by the downregulation of complement components C1q, C3, C5, C9, and the modulation of macrophage infiltration and pro-inflammatory cytokine release through the C5a/C5aR1 axis. Gene set enrichment analysis further suggested that YYJH can alleviate AP-related metabolic disorders and immune dysregulation. Molecular biology experiments demonstrated that after YYJH intervention, the complement cascade reaction was significantly inhibited, with downregulated expression levels of C5a and C5aR1, and decreased membrane localization signals of the macrophage marker F4/80, along with reduced expression levels of inflammatory factors.</p><p><strong>Conclusions: </strong>Research indicates that YYJH exerts anti-inflammatory effects by regulating the classical complement pathway and the C5a/C5aR1 axis, inhibiting the production of inflammatory mediators and the activation of immune cells. This provides a theoretical basis for the molecular mechanisms underlying traditional Chinese medicine in the treatment of acute pharyngitis.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"134"},"PeriodicalIF":5.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12376329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944897","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":"Multi-omics analysis reveals ACOT1 as the key target of piperine in Piper Longum-mediated gastric cancer treatment.","authors":"Boyu Pan, Ling Liu, Xiaofeng Wang, Runfang Wang, Zeyang Liu, Xiaoyan Li, Bao Jin, Jie Zhang, Rui Li, Liren Liu, Chunnuan Wu","doi":"10.1186/s13020-025-01186-y","DOIUrl":"10.1186/s13020-025-01186-y","url":null,"abstract":"<p><strong>Background: </strong>Piper longum demonstrates significant therapeutic potential against gastric cancer (GC), but its underlying mechanisms remain incompletely understood. This study aimed to establish a comprehensive multi-omics framework to elucidate Piper longum's anti-cancer mechanisms.</p><p><strong>Methods: </strong>We integrated in vivo experiments, metabolomics, gut microbiota analysis, mass spectrometry, and network pharmacology to investigate Piper longum's effects. In vivo studies assessed its dose-dependent inhibition of GC growth compared to standard chemotherapy (L-OHP + 5-FU). Metabolomics identified altered lipid metabolism pathways, while gut microbiota analysis evaluated its impact on microbial composition. Piperine was identified as the key active compound, and ACOT1 was pinpointed as a critical molecular target through integrated analysis.</p><p><strong>Results: </strong>Piper longum significantly suppressed gastric cancer (GC) growth in a dose-dependent manner, with high-dose treatment demonstrating superior efficacy compared to conventional chemotherapy (L-OHP + 5-FU). Metabolomic analysis revealed that its anti-cancer mechanism primarily involves the reprogramming of lipid metabolism pathways in GC cells, while gut microbiota assessment confirmed that it modulates intestinal flora composition without compromising microbial diversity, supporting its favorable safety profile. Mass spectrometry identified piperine as the key bioactive compound, and integrated metabolomics and network pharmacology further pinpointed ACOT1 as a critical molecular target, which interacts with piperine that confirmed by CETSA. Notably, high ACOT1 expression was associated with poor prognosis in GC patients, underscoring its therapeutic relevance.</p><p><strong>Conclusions: </strong>This study elucidates Piper longum's \"component-target-pathway\" mechanism in GC treatment, highlighting piperine-ACOT1-de novo lipogenesis regulatory pathway as a critical axis. Additionally, it establishes a robust multi-omics framework for evaluating traditional medicine efficacy, providing a theoretical foundation for Piper longum's clinical application in GC therapy.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"133"},"PeriodicalIF":5.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12376458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944963","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}