Chinese Medicine最新文献

{"title":"Buyang Huanwu Decoction promotes neurorepair after spinal cord injury through a Lactobacillus johnsonii-indole-3-lactic acid-AhR-PI3K/Akt axis.","authors":"Jinwang Dong, Yang Cao, Xiujin Chen, Tao Xie, Xiaobo Zhang, Qingpeng Zhao, Cunhu Shi, Qiangqiang Miao, Zhengwei Xu, Liang Yan, Liang Dong","doi":"10.1186/s13020-026-01408-x","DOIUrl":"https://doi.org/10.1186/s13020-026-01408-x","url":null,"abstract":"<p><strong>Background: </strong>Spinal cord injury (SCI) induces gut microbiota dysbiosis, which significantly affects recovery. Buyang Huanwu Decoction (BHD), a traditional Chinese medicine formula, has shown therapeutic effects on SCI. Although BHD is known to modulate gut microbiota, whether its benefits are mediated through the gut-spinal cord axis remains unclear.</p><p><strong>Methods: </strong>A rat SCI model was established. BHD was administered orally, and fecal microbiota transplantation (FMT) from BHD-treated rats (BHD-FMT) was performed to assess neuroprotective and gut-protective effects. Behavioral testing, histology, and immunofluorescence evaluated motor recovery, inflammation, and neuroregeneration. Gut microbiota profiling was performed using 16S rDNA sequencing and metagenomics, while targeted metabolomics quantified tryptophan metabolites. Transcriptomics validated key pathways, and a microbiota-metabolite-signaling network was constructed.</p><p><strong>Results: </strong>BHD significantly improved motor function, reduced spinal inflammation, and promoted neuronal survival and axonal regeneration. It restored gut function, reduced colonic inflammation, and enhanced ZO-1 and Occludin expression, which were further confirmed by FMT. BHD-FMT reshaped the gut microbiota and enriched Lactobacillus johnsonii, which correlated positively with recovery. Metabolomics showed increased tryptophan metabolites, including indole-3-lactic acid (ILA) and indole-3-propionic acid (IPA), with ILA strongly associated with functional improvement. Transcriptomic analysis and Western blot validation demonstrated that BHD-FMT activated the AhR-PI3K/Akt pathway, which was suppressed by an AhR antagonist.</p><p><strong>Conclusion: </strong>BHD promotes neuroregeneration after SCI by reshaping gut microbiota and enhancing tryptophan metabolism, potentially exerting its effects through the L. johnsonii-ILA-AhR-PI3K/Akt network. These findings reveal a gut-spinal cord axis-mediated mechanism of BHD and highlight microecological targets for SCI therapy.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834357","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":"Research progress on the mechanisms of Panax ginseng and its active components in maintaining skin homeostasis and disease intervention.","authors":"Lu Ding, Zihan Wang, Nanqi Hou, Yuchi Zhou, Hongyu Qi, Zirui Li, Xueyan Li, Jiaojiao Xue, Siyu Song, Zeyu Wang, Daqing Zhao, Rui Jiang, Xiangyan Li","doi":"10.1186/s13020-026-01407-y","DOIUrl":"https://doi.org/10.1186/s13020-026-01407-y","url":null,"abstract":"<p><p>Panax ginseng (Panax ginseng C.A. Meyer) is a classic herbal medicine widely utilized in dermatological management, yet its precise therapeutic mechanisms have only recently begun to be fully elucidated. This review systematically synthesizes the pharmacological roles of ginseng's active components, including ginsenosides, polysaccharides, and gintonin, in maintaining skin homeostasis and treating various cutaneous pathologies. Emerging evidence suggests that the efficacy of ginseng extends beyond direct molecular interactions, exhibiting the distinct characteristics of \"indirect pharmacology.\" Specifically, parent ginsenosides function primarily as natural prodrugs that require microbial biotransformation into high-affinity active metabolites, such as Compound K and Rh2, to exert potent therapeutic effects. Functionally, these components regulate skin health by mobilizing endogenous host defense systems, particularly through the activation of the Nrf2/ARE antioxidant pathway and the suppression of inflammatory cascades via the NF-κB, MAPK, and IL-1 signaling networks. Furthermore, they remodel the systemic microenvironment through the gut-skin axis, facilitating metabolic homeostasis to improve skin barrier function. Notably, biotransformation rates and ultimate therapeutic efficacy are highly dependent on individualized variables, such as host age, dietary patterns, and baseline disease states. This systemic regulation has demonstrated robust efficacy in intervening in complex pathologies, including atopic dermatitis, psoriasis, and skin cancer. Additionally, this article addresses the translational bottleneck of low bioavailability and evaluates recent advances in novel skin delivery systems, specifically those utilizing ginseng-derived exosomes. Collectively, this review provides a scientific framework for understanding the systemic actions of ginseng, supporting its development as a precision botanical therapy for dermatological applications.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834369","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":"Shuangshen granules enhance anti-PD1 therapy effectiveness in lung adenocarcinoma by modulating myeloid-derived suppressor cell-induced T cell exhaustion.","authors":"Zhong-Ning He, Qi Huang, Yi Li, Jia-Qi Hu, Tong-Tong Liu, Yu-Wei Zhao, Xiao-Ling Ren, Shu-Lin He, Yue Li, Bo-Lun Shi, Rui Liu, Qiu-Jun Guo, Xing Zhang, Zhan Shi, Jie He, Run-Zhi Qi, Bao-Jin Hua","doi":"10.1186/s13020-026-01391-3","DOIUrl":"10.1186/s13020-026-01391-3","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Worldwide, lung cancer is the most common cause of cancer-related deaths. Molecular targeted therapies and immunotherapies for non-small-cell lung cancer (NSCLC) have improved outcomes markedly over the past two decades. However, the vast majority of advanced NSCLCs become resistant to current treatments and eventually progress. A traditional Chinese medicine (TCM) formula of Shuangshen granules (SSG) has demonstrated potential in alleviating cancer side effects and improving survival rate. Despite clinical evidence supporting its benefit, there is still insufficient understanding of the active compounds in SSG and their underlying mechanisms, which limits its broader clinical application.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Lewis lung carcinoma (LLC) tumor-bearing mouse model was established to assess the efficacy of combined SSG and anti-PD-1 therapy in vivo, and myeloid-derived suppressor cells (MDSC) and CD8&lt;sup&gt;+&lt;/sup&gt;T cells were isolated for in vitro co-culture experiments, while pathological examination was conducted using hematoxylin and eosin (HE). The expression of PD-1, TIM-3, CTLA-4, LAG-3, Arg-1, IDO, iNOS, PD-L1 and Gal-9 was detected using immunohistochemistry (IHC), immunofluorescence, and flow cytometry and Western blotting. The expression of IL-2, TNF-α and IFN-γ were detected by reverse transcription-quantitative polymerase chain reaction (qPCR). Concentrations of IL-10 and TGF-β were measured by enzyme-linked immunosorbent assay (ELISA). Network pharmacology and molecular docking were utilized to screen for potential therapeutic targets and intervening signaling pathways of SSG in lung adenocarcinoma (LUAD). The predictions derived from this approach were further verified using Western blotting.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;In vivo experiments using LLC xenograft mice demonstrated that SSG suppressed tumor growth in a dose-dependent manner, with high-dose SSG showing optimal efficacy in inhibiting tumor angiogenesis and cell proliferation. SSG enhances anti-tumor immunity by reducing T cell exhaustion and MDSC-mediated immunosuppression, with SSG + anti-PD-1 combination therapy synergistically optimizing the tumor immune microenvironment. Network pharmacology analysis revealed 5 hub targets (IL2, STAT3, HSP90AA1, LGALS3, and FGF2) associated with immune, LUAD, and active ingredients of SSG, with significant enrichment in the PI3K-Akt pathway. Compared with the control group, the protein expression levels of p-PI3K and p-Akt in the SSG group were significantly down-regulated, indicating that the PI3K-Akt pathway may be inhibited.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;SSG could dose-dependently inhibit LLC tumor growth in mice and exert antitumor effects by alleviating T-cell exhaustion and MDSC-mediated immunosuppression. Notably, IL2, STAT3, HSP90AA1, LGALS3 and FGF2, as potential targets of SSG, were significantly enriched in the PI3K-Akt pathway, which provide a novel perspective for the treatme","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834412","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":"TRPV1 in skeletal muscles mediates the improvement of cardiac function induced by acupuncture at the PC6 acupoint in rats with acute myocardial infarction.","authors":"Xue Liu, Yongjian Wu, Yongxiao Zhai, Weifang Gao, Xiaoyu Meng, Wubo Pei, Yuxin Fang, Yi Guo, Yangyang Liu","doi":"10.1186/s13020-026-01384-2","DOIUrl":"10.1186/s13020-026-01384-2","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;The acupoint is the initial response site to acupuncture stimulation, and changes in the acupoint affect the subsequent therapeutic effects of acupuncture. However, the mechanism of acupuncture from this initial site has not yet been clarified. Based on an experimental model of acupuncture at Neiguan (PC6) for intervening in acute myocardial infarction (AMI), this study aimed to 1) investigate whether acupuncture-induced local muscle contraction at the PC6 acupoint mediates the therapeutic effect of acupuncture, and 2) explore the initiation mechanism of acupuncture's effect from the perspective of transient receptor potential vanilloid 1 (TRPV1).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Sprague-Dawley (SD) rats were used to establish the AMI model via ligation of the left anterior descending coronary artery (LAD). 1.To identify the key tissue layer mediating acupuncture efficacy: SD rats were randomly divided into the Sham group, AMI group, AMI + acupuncture at muscle-layer (ACU-M) group, and AMI + acupuncture at subcutaneous-layer (ACU-S) group. Cardiac function was evaluated using a small animal ultrasound imaging system; myocardial ischemic area was measured via 2,3,5-triphenyltetrazolium chloride (TTC) staining, and serum norepinephrine (NE) levels were detected using an enzyme-linked immunosorbent assay (ELISA) kit. 2.To verify the role of muscle contraction: Another cohort of SD rats was randomly divided into the Sham + Vehicle (0.9% sodium chloride, NaCl) group, AMI + Vehicle group, AMI + Vehicle + acupuncture group and AMI + succinylcholine chloride (Scc, muscle relaxant) + acupuncture group. Acupuncture was performed post-AMI modeling, with the same efficacy indexes as above. Additionally, PC6 tissue and C5-T1 segmental dorsal root ganglia (DRG) were collected from each group. Immunofluorescence (IF) staining and western blot (WB) analysis were used to detect TRPV1 expression in the acupoint muscle layer and TRPV1-positive neuron activation in DRGs. 3. To clarify the role of TRPV1: a TRPV1 inhibitor was microinjected into the PC6 muscle layer before acupuncture; changes in TRPV1 (acupoint/DRGs), cardiac function, myocardial ischemic area, and serum NE were measured to evaluate the relationship between acupuncture effect and TRPV1.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Both the acupuncture at muscle and subcutaneous layer improved cardiac function, reduced the area of myocardial ischemia, and lowered serum NE levels in AMI rats, however the modulatory effect of acupuncture at muscle layer was more pronounced in AMI rats. PC6 injection of Scc followed by acupuncture reversed the modulatory effect of acupuncture on AMI rats. WB and IF results both showed that compared with the AMI group, TRPV1-positive area of the muscle layer in the acupoint area, protein expression as well as activated TRPV1-positive neurons in the DRG were significantly increased, while with the use of Scc followed by acupuncture, TRPV1-positive express","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834444","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 stabilized enrichment method for rosemary diterpenoids and their therapeutic potential in diabetic kidney disease.","authors":"Jiali Wei, Qian Xiao, Hua Yang, Fei Li, Ping Li","doi":"10.1186/s13020-026-01404-1","DOIUrl":"10.1186/s13020-026-01404-1","url":null,"abstract":"<p><strong>Background: </strong>As a traditional medicinal herb, rosemary leaves have shown potential for the treatment for diabetic kidney disease (DKD). However, the bioactive compounds responsible for its anti-DKD effects remain unidentified, and the instability of its primary phytochemicals limits its practical application.</p><p><strong>Methods: </strong>This study investigated the active components of rosemary leaves and characterized their degradation pathways using UPLC-Q/TOF-MS/MS. Four solvent-extracted fractions were evaluated using an in vitro DKD model to identify the major anti-DKD constituents. A targeted enrichment method was then developed to isolate these bioactive compounds. Finally, a DKD model was established in C57BL/6J mice using high-fat diet combined with streptozotocin injection to evaluate the therapeutic effects of the enriched extracts. The pharmacokinetic profiles of the major components of TD were further investigated.</p><p><strong>Results: </strong>38 chemical constituents were characterized with diterpenoids were identified as the primary anti-DKD constituents by in vitro DKD model. Considering their pronounced susceptibility to oxidative degradation, a novel enrichment strategy for total diterpenoids (TD) was developed based on water and ethanol. Vitamin C served as a stabilizer to improve TD stability, leading to a TD extraction yield of 40.12% and the diterpenoid content of 81.80%. In vivo studies revealed that TD attenuated renal injury, improved glucose and lipid dysmetabolism, and reduced renal oxidative stress in DKD mice. The in vivo absorption profiles showed that TD also exhibited good bioavailability.</p><p><strong>Conclusion: </strong>This study provides an effective method for TD enrichment and demonstrates the renoprotective effects of TD. These findings offer new insights on the broader use of rosemary leaves and the development of natural product-based therapies for DKD.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147855/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834428","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":"Chemical proteomics reveals sinomenine's anti-inflammatory mechanism through serum protein covalent modification.","authors":"Meixian Liu, Zhiyuan Zheng, Yida Zhang, Xiqing Bian, Yue Zhuo, Hai-Ying Wu, Jian-Lin Wu, Na Li","doi":"10.1186/s13020-026-01403-2","DOIUrl":"https://doi.org/10.1186/s13020-026-01403-2","url":null,"abstract":"<p><strong>Background: </strong>Covalent protein modification by drugs or their reactive metabolites has emerged as an important mechanism underlying pharmacological activity. However, its contribution to the therapeutic effects of compounds derived from traditional Chinese medicine remains insufficiently characterized. Sinomenine (SIN), an active alkaloid from Sinomenium acutum, has long been utilized in managing inflammatory disorders, yet the molecular basis of its efficacy is not fully elucidated.</p><p><strong>Methods: </strong>A discovery-driven chemical proteomics approach was deployed to investigate the role of covalent protein modification in the action of SIN. Metabolite profiling and in vitro reactivity assays were initially conducted to evaluate the modification potential of SIN and its metabolites. Subsequently, in vivo serum proteomics analysis in rat was performed to map the covalent modification landscape. Enriched biological pathways were identified through bioinformatics analyses, and functional validation was executed using western blotting and enzymatic activity assays.</p><p><strong>Results: </strong>Results demonstrated that SIN, along with its oxygenated and demethylated metabolites, could covalently modify cysteine and lysine residues on proteins via three distinct modification patterns. Serum proteomics analysis identified seven proteins modified by SIN in vivo. Pathway enrichment analysis revealed that these target proteins were predominantly involved in coagulation and complement pathways. Functional validation demonstrated that SIN treatment significantly suppressed the activation of the coagulation cascade, the kallikrein-kinin system (KKS), and the complement cascade.</p><p><strong>Conclusions: </strong>This study provides evidence that covalent protein modification may contribute to the pharmacological effects of SIN by modulating coagulation and complement pathways, which are implicated in inflammatory regulation. The findings offer new mechanistic insights into SIN's action and underscore the utility of covalent proteomics as an effective strategy for uncovering the molecular mechanisms of bioactive compounds derived from traditional Chinese medicine.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13130404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811976","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":"Shexiang Tongxin Dropping Pills targeting Piezo1/Ca²⁺/NLRP3 axis attenuates vascular endothelial inflammation.","authors":"Jingya Liu, Ke Wang, Hongjing You, Liang Long, Yue Xu, Qiuhe Chen, Yang Chen","doi":"10.1186/s13020-026-01402-3","DOIUrl":"10.1186/s13020-026-01402-3","url":null,"abstract":"<p><strong>Background: </strong>Vascular endothelial inflammation is a key pathological process underlying various inflammatory vascular conditions, which can lead to severe cardiovascular complications. Shexiang Tongxin Dropping Pills (STDP) is a traditional Chinese medicine formulation clinically used for cardiovascular disorders and has shown protective effects on the vascular endothelium. However, the specific mechanisms by which STDP attenuates vascular endothelial inflammation remain incompletely elucidated.</p><p><strong>Methods: </strong>An experimental model of LCWE-induced vasculitis was established by intraperitoneal injection of lactobacillus casei cell wall extract (LCWE) in C57BL/6 mice. The effects of STDP were evaluated through whole blood analysis, EVG staining, and immunofluorescent staining for adhesion molecules (ICAM-1, VCAM-1) and macrophage infiltration. An in vitro endothelial damage model was established by stimulating murine vascular endothelial cells (MVECs) with LCWE. Network pharmacology, calcium imaging, and siRNA-mediated knockdown of Piezo1 were employed to elucidate the underlying mechanism.</p><p><strong>Results: </strong>STDP greatly alleviated the weight loss and reduced spleen coefficient in LCWE-induced mice. It decreased the proportion of monocytes in the blood, reduced the area and maximum diameter of the abdominal aorta, and preserved the structural integrity of elastic fibers in the abdominal aorta wall as revealed by EVG staining. Besides, STDP significantly alleviated vascular endothelial inflammation both in the mouse model and in the cell model, as manifested by inhibition of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression. Mechanistically, STDP significantly inhibited Piezo1 channel activation, thereby reducing calcium ion (Ca²⁺) influx. This inhibitory effect prevented the activation of the NLRP3 inflammasome in endothelial cells, thus protecting endothelial cells and alleviating inflammation.</p><p><strong>Conclusion: </strong>STDP attenuates vascular inflammation by downregulating Piezo1 expression, thereby reducing Ca²⁺ influx and suppressing NLRP3 inflammasome activation. The Piezo1/Ca²⁺/NLRP3 pathway may represent a novel therapeutic target for ameliorating vascular endothelial inflammation.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting tumor-associated macrophages through phytochemicals: a promising strategy for cold tumor therapy.","authors":"Tian Shue, Yujun Guo, Peishan Zhou, Dan Yao, Huan Liao, Chengxin Long, Yulin Qi, Luyao Yang, Nianzhi Chen","doi":"10.1186/s13020-026-01401-4","DOIUrl":"10.1186/s13020-026-01401-4","url":null,"abstract":"<p><p>Immunotherapy serves as the fourth modality for cancer treatment, following surgery, radiotherapy, and chemotherapy. However, its efficacy remains inconsistent due to the heterogeneity of the tumor microenvironment (TME). Tumors characterized by an immunosuppressive TME that are unresponsive to immunotherapy are termed \"cold tumors.\" Thus, strategies to reverse this immunosuppressive environment are promising for treating cold tumors. Tumor-associated macrophages (TAMs) play a significant role in this process, making TAM-targeting therapies potentially valuable. Natural products (NPs), which are bioactive compounds from traditional herbs, exhibit broad anticancer effects and modulate TAM polarization, positioning them as a promising source for anticancer agents. This article explores the relationship between TAMs and the TME, emphasizing the mechanisms by which natural products, such as terpenoids and quinones, influence TAM polarization to inhibit tumor progression. By analyzing TAM roles in the TME and summarizing existing natural products targeting TAM polarization, this study offers insights for developing novel TAM-targeting drugs, and aids in the conversion of cold tumors to hot tumors.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764251","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":"Qinggan Jianpi formula attenuates atherosclerosis by suppressing macrophage lactate transport to activate repair genes via H3K18 lactylation.","authors":"Xuefeng Zhuang, Rui Zhang, Jiatong Sun, Wenli Song, Jing Wang, Yvna Han, Jinji Wang, Hongzhu Chen, Zhijie Zhu, Weijia Liu, Lijing Li","doi":"10.1186/s13020-026-01394-0","DOIUrl":"https://doi.org/10.1186/s13020-026-01394-0","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis (AS) is a complex vascular disease characterized by lipid accumulation, chronic inflammation, and immune dysregulation. Qinggan Jianpi Formula (QGJP), a traditional Chinese medicinal preparation, is widely used for treating lipid metabolism disorders. However, the mechanisms of action and active components remain unclear. These uncertainties restrict its clinical use and necessitate systematic research to clarify them. This study aims to investigate the therapeutic effects of QGJP on AS and to elucidate the role of suppressing macrophage M1 polarization in this process, mediated by the regulation of lactate transport and the promotion of histone lactylation.</p><p><strong>Methods: </strong>In this study, first, major chemical components of QGJP were identified via UHPLC-HRMS. We employed a high-fat diet (HFD) fed ApoE^⁻/⁻ C57BL/6 mice to establish an AS model, along with in vitro models of ox-LDL-induced lipid injury in HUVECs and ox-LDL-induced foam cell formation in THP-1, followed by QGJP treatment. We elucidated the therapeutic effects and underlying mechanisms of QGJP in AS through multiple approaches, including protecting endothelial cells and regulating macrophage polarization.</p><p><strong>Results: </strong>QGJP significantly reduced blood lipids, modulated plaque lipid and collagen content, and alleviated aortic pathological damage in AS mice. Moreover, QGJP downregulated the expression of matrix metalloproteinases, adhesion molecules, and chemokines, enhanced endothelial migration capacity, and inhibited monocyte-endothelial adhesion. Further analysis of macrophage polarization phenotypes revealed that QGJP significantly modulated their polarization state. Mechanistically, QGJP suppressed the expression of key glycolytic enzymes while promoting that of FH. Consequently, it reversed the increase in glycolytic activity observed in macrophages during atherosclerosis. Furthermore, QGJP regulated lactate transport by suppressing MCT4 expression. This modulation orchestrated histone H3K18 lactylation, which in turn activated repair-related gene programs in macrophages. Through UHPLC-HRMS analysis, 47 bioactive constituents of QGJP were identified. Experimental validation confirmed that SAA, LA, and CAB effectively inhibited M1 macrophage polarization and activated the expression of proteins related to reparative genes.</p><p><strong>Conclusions: </strong>This study establishes the critical role of metabolic reprogramming and epigenetic regulation in AS progression. Our findings suggest that a mechanism whereby QGJP alleviates AS may involve the inhibition of the HIF-1α/MCT4 axis and lactate transport, which regulates histone H3K18 lactylation to promote a reparative macrophage phenotype.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13107618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764182","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":"FeiyanHeji multifunctionally inhibits influenza virus via PA protein degradation and RIG-I signaling pathway potentiation.","authors":"Tongtong Cao, Wenqiang Sun, Yan Hu, Chang Liu, Yue Hou, Jing Shu, Ningning Zhang, Qiang He, Wenxian Yang","doi":"10.1186/s13020-026-01372-6","DOIUrl":"https://doi.org/10.1186/s13020-026-01372-6","url":null,"abstract":"<p><p>Influenza virus infection can lead to high mortality and severe disease complicated by secondary bacterial pneumonia. FeiyanHeji (FyHj) is a traditional Chinese medicine (TCM) mixture used clinically to treat pneumonia caused by influenza, although its mechanism of action remains unclear. We first conducted a network pharmacology analysis of the ten components in FyHj to predict their potential interactions with influenza-related targets. GO and KEGG analyses revealed significant enrichment in the inflammatory response, ubiquitin protein binding, RNA virus-related pathways, and the RIG-I signaling pathway, suggesting these may be involved in the anti-influenza process. Further experimental validation demonstrated that FyHj inhibits viral replication through two mechanisms: (1) promoting the degradation of polymerase acidic (PA) protein by interfering with UBP11-mediated K48-linked deubiquitination, and (2) enhancing antiviral innate immunity by upregulating the RIG-I/MAVS signaling pathway and stabilizing MAVS through inhibition of TRIM25-mediated K48-linked ubiquitination of MAVS. Finally, FyHj was observed to reduce lung viral load and inflammation in mice infected with influenza A virus (IAV). In conclusion, FyHj decoction elicits potent antiviral effects through multiple mechanisms, providing a mechanistic basis for the clinical application of FyHj and highlighting its potential as a source for multi-target anti-influenza therapies.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13101370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764204","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}