Chinese Medicine最新文献

{"title":"Eerdun Wurile, a Mongolian medicine, alleviates neuronal damage and improves neurological dysfunction after cerebral hemorrhage by activating the PI3K/AKT signaling pathway.","authors":"Wenhui Yang, Yilu Li, Xueying Wang, Yushi Tang, Zhenxing Tao, Pengpeng Li, Shiqing Du, Zhenqian Mu, Xiaojie Lu, Xudong Zhao","doi":"10.1186/s13020-026-01459-0","DOIUrl":"10.1186/s13020-026-01459-0","url":null,"abstract":"<p><strong>Background: </strong>This study aims to evaluate the neuroprotective effects of the Mongolian medicine Eerdun Wurile (EW) against intracerebral hemorrhage (ICH) and explore its underlying mechanisms. ICH, a severe subtype of stroke, is characterized by a complex pathological process, with no specific treatments currently available. EW, a traditional Mongolian medicinal formula, has a long history of use in treating central nervous system disorders, but its mechanism of action in ICH remains poorly understood.</p><p><strong>Methods: </strong>A mouse model of ICH was induced through stereotactic intracerebral injection of Collagenase Type IV. Behavioral assessments, histological examinations, and RNA sequencing were conducted to assess the effects of EW and elucidate its mechanism of action in mitigating neuronal injury post-cerebral hemorrhage.</p><p><strong>Results: </strong>EW administration improved a range of ICH-induced deficits, including neurological and neurofunctional impairments, anxiety-like behaviors, and cognitive dysfunction. EW protected neurons from injury and apoptosis in both in vitro and in vivo models. Additionally, EW treatment suppressed the activation of astrocytes and microglia, reducing neuroinflammation, preserving blood-brain barrier integrity, and alleviating synaptic damage. RNA-seq analysis revealed that the PI3K/AKT signaling pathway plays a key role in EW's neuroprotective effects. EW activates this pathway, modulating the balance of Bcl-2 family proteins, thereby reducing neuronal apoptosis.</p><p><strong>Conclusion: </strong>EW confers neuroprotection through multiple mechanisms. These findings provide strong experimental evidence supporting the potential clinical application of EW as a therapeutic agent for ICH.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13340406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403922","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":"Shengxian decoction suppresses malignant progression of lung adenocarcinoma by enhancing CD8⁺ T cell function via the FYN-PI3K/AKT axis.","authors":"Qiong Ma, Xiao Zeng, Chunxia Huang, Xingyue Liu, Jiawei He, Yuting Bai, Yuxuan Xiong, Shiyan Tan, Zongyi Mao, Xueke Li, Qian Wang, Xi Fu, Fengming You, Yifeng Ren, Chuan Zheng","doi":"10.1186/s13020-026-01442-9","DOIUrl":"10.1186/s13020-026-01442-9","url":null,"abstract":"<p><strong>Background: </strong>Shengxian Decoction (SXD), a traditional Chinese herbal formula, has demonstrated significant clinical efficacy against lung adenocarcinoma (LUAD). However, its exact mechanisms of action remain to be elucidated. This study aimed to establish an animal model capable of simulating the dynamic progression of LUAD to investigate the anti-tumor effects and immunomodulatory mechanisms of SXD.</p><p><strong>Methods: </strong>A TK (Trp53^-/-; Kras^G12D) LUAD mouse model was established by subcutaneously transplanting CRISPR/Cas9-edited mouse lung organoids into immunocompetent C57BL/6 mice. The model was characterized by histopathology, RT-qPCR, T7E1 assay, and transcriptomic analysis. Potential mechanisms of SXD were investigated through an integrated approach combining UHPLC-MS/MS, network pharmacology, molecular docking, and eQTL-based Mendelian randomization. Core targets and key signaling pathways were further evaluated by in vivo transcriptomic analysis, multiplex immunofluorescence, flow cytometry, an in vitro CD8⁺ T-cell coculture model, and surface plasmon resonance (SPR) analysis.</p><p><strong>Results: </strong>An immunocompetent TK-LUAD mouse model was successfully established, showing the dynamic pathological progression of LUAD and accompanying changes in immune infiltration. SXD treatment significantly delayed malignant progression in this model and was associated with modulation of the tumor immune microenvironment, as reflected by increased CD8⁺ T-cell infiltration and elevated levels of the cytotoxic effector molecules TNF-α, IFN-γ, and GZMB. Integrative analyses prioritized FYN as a candidate target potentially involved in SXD-mediated immunomodulation. SPR analysis showed concentration-dependent binding of representative SXD-derived compounds, including secoisolariciresinol, berberine, and acacetin, to FYN, providing additional support for direct target engagement. Further in vivo and in vitro experiments indicated that SXD enhanced the cytotoxic function of CD8⁺ T cells by activating the FYN-PI3K/AKT signaling pathway.</p><p><strong>Conclusion: </strong>This study establishes an immunocompetent animal model for investigating LUAD progression and associated changes in the tumor immune microenvironment. In addition, this study provides evidence suggesting that the antitumor activity of SXD may be associated with FYN-related activation of the PI3K/AKT signaling pathway and subsequent enhancement of CD8⁺ T cell function. These findings provide a theoretical and experimental basis for further investigation of SXD as a potential therapeutic strategy for LUAD.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13335393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396167","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 systems herbal-to-molecule and transcriptomic strategy identifies emodin as an ESR1-targeting phytochemical driving thrombopoiesis.","authors":"Xiao Qi, Qinyao Li, Fengyu Li, Linglin Zhou, Qi Mo, Jing Zeng, Tianci Hu, Sheng Liu, Xinyue Mei, Min Wu, Xuejing Qiang, Qiyang Cheng, Anguo Wu, Xiaogang Zhou, Feihong Huang, Qiaozhi Wang, Peng Chen, Jianming Wu, Long Wang","doi":"10.1186/s13020-026-01454-5","DOIUrl":"10.1186/s13020-026-01454-5","url":null,"abstract":"<p><p>Radiation-induced thrombocytopenia (RIT) is a major dose-limiting toxicity of radiotherapy, for which effective pharmacological interventions remain limited. Rhei Radix et Rhizoma (RR) is widely used in traditional medicine, yet its thrombopoietic activity and molecular basis have not been systematically defined. Here, we investigated the effects of RR on thrombopoiesis using an integrated herbal-to-molecule and transcriptomic strategy. RR extract and representative phytochemicals were screened for megakaryocyte (MK) differentiation in Meg-01, K562, and murine haematopoietic stem and progenitor cells (HSPCs), followed by validation in a mouse RIT model. Network pharmacology and transcriptomic analyses indicated that RR regulates thrombopoiesis through coordinated multi-pathway modulation. Emodin was identified as the principal bioactive constituent mediating these effects. Functionally, emodin promoted MK maturation and polyploidization in vitro, accelerated megakaryopoiesis and platelet recovery in irradiated mice. Integrated target prediction and experimental validation identified ESR1 as a direct functional target of emodin, supported by molecular docking, molecular dynamics simulations, CETSA, and DARTS assays. Mechanistically, emodin activated ESR1-dependent PI3K/AKT and JAK2/STAT3 signaling, leading to induction of lineage-specific transcription factors and enhanced platelet biogenesis. Collectively, these findings identify emodin as a key thrombopoietic constituent of RR and reveal an ESR1-centered regulatory axis in megakaryopoiesis, supporting its therapeutic potential for RIT.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13335142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396129","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":"Wubi Shanyao Pills ameliorate glucocorticoid-induced osteoporosis by regulating bone marrow T cell homing as an immune intermediate to restore bone metabolism.","authors":"Ying-Jie Dong, Jia-Yue Zhu, Jie Su, Ya-Wen Sun, Er-Xiao Chen, Xiao-Hu Jin, Gui-Yuan Lv, Su-Hong Chen","doi":"10.1186/s13020-026-01452-7","DOIUrl":"10.1186/s13020-026-01452-7","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;The disruption of bone immune function and bone metabolism homeostasis is intricately linked to the onset and progression of glucocorticoid-induced osteoporosis (GIOP). From the perspective of indirect pharmacology, bone immune cells act as critical intermediate mediators that bridge systemic drug exposure and local bone tissue responses. Wubi Shanyao Pills (WBSY), a Chinese patent medicine, have been shown to modulate T lymphocyte levels in naturally aging mice and improve bone strength. However, whether WBSY exerts anti-GIOP effects through an indirect immunomodulatory pattern and its underlying intermediate mechanisms remain unclear.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Purpose: &lt;/strong&gt;This study aims to elucidate the effects and mechanisms of WBSY on GIOP in mice.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Initially, the chemical constituents of WBSY were characterized using high-performance liquid chromatography (HPLC). Following this, a GIOP mouse model was developed through intraperitoneal administration of dexamethasone at a dosage of 10 mg/kg every three days. The mice were subsequently treated with WBSY at varying dosages-high (1.5 g/kg), medium (0.75 g/kg), and low (0.375 g/kg)-via gavage over a 20-week duration. Throughout the experimental period, general physiological parameters of the mice were systematically monitored. Bone mass alterations were subsequently assessed through bone strength measurements, micro-computed tomography analysis of bone tissue, and histopathological examination. Potential target pathways were identified via transcriptomic analysis. Furthermore, bone immunology-related parameters were evaluated using flow cytometry, including the proportion of T lymphocytes in the spleen and bone marrow, as well as the expression levels of the CXC chemokine ligand 10-chemokine receptor 3 (CXCL10-CXCR3) axis. Concurrently, key indicators of the bone metabolism pathway, such as the Receptor Activator of Nuclear Factor-κB (RANK), Receptor Activator of Nuclear Factor-κB ligand (RANKL), and osteoprotegerin (OPG), were further analyzed.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The results of the HPLC analysis demonstrated that the concentrations of echinacoside, acteoside, and schisandrol in WBSY were 7.82 mg/g, 2.18 mg/g, and 0.32 mg/g, respectively. Subsequently, the findings revealed that WBSY significantly enhanced general physiological parameters, including body weight, grip strength, and anal/back temperature, in GIOP mice. WBSY not only enhanced bone strength and mitigated pathological damage to the femur, but also significantly improved bone microarchitecture. This improvement was evidenced by an increase in bone volume/tissue volume, trabecular thickness, and trabecular number, alongside a reduction in trabecular separation and the structural model index. Furthermore, transcriptomic analysis indicated that WBSY may exert anti-GIOP effects by modulating key pathways, including osteoclast differentiation, interleukin-17A (IL-17A), a","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374770","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":"Pro-EGCG suppresses endometriosis progression via regulating monocytic myeloid-derived suppressor cells.","authors":"Qianhan Xu, Lu Chen, Jun Chen, Haoyue Hu, Zhihua Luo, Zhentao Gong, Yee Lee Ng, Jinchuan Liu, Sze Wan Hung, Yi Song, Nga Ping Ip, See Yung Chau, Yonggang Duan, Chi Chiu Wang, Ting Guo, Kam Tong Leung, Jingying Zhou, Pui Wah Chung, Tao Zhang","doi":"10.1186/s13020-026-01451-8","DOIUrl":"10.1186/s13020-026-01451-8","url":null,"abstract":"<p><strong>Background: </strong>Pro-EGCG has shown therapeutic promise for endometriosis, yet its immunoregulatory mechanisms remain unclear. Myeloid-derived suppressor cells (MDSCs) are key drivers of disease progression. This study investigates whether Pro-EGCG alleviates endometriosis by modulating MDSC-mediated immune and stromal dysregulation.</p><p><strong>Methods: </strong>The therapeutic effects of Pro-EGCG were evaluated in an experimental endometriosis mouse model by assessing lesion burden, histology, and MDSC dynamics. The functional necessity of monocytic MDSCs (M-MDSCs) was validated via adoptive transfer. Clinical relevance was assessed in peripheral blood and lesions from women with or without endometriosis via flow cytometry and multiplex immunofluorescence staining. Furthermore, the direct effects of Pro-EGCG on human PBMC-derived M-MDSCs were examined in vitro, including their immunosuppressive function and their ability to promote fibrosis in a co-culture system with human endometriotic stromal cells.</p><p><strong>Results: </strong>In the mouse model, Pro-EGCG treatment significantly reduced lesion weight, volume, and fibrosis, accompanied by consistent M-MDSC reduction systemically and locally. Lesion-infiltrating M-MDSCs, rather than polymorphonuclear MDSCs (PMN-MDSCs), positively correlated with disease severity. Adoptive transfer of M-MDSCs reversed Pro-EGCG's therapeutic effects. In clinical samples, data confirmed a significant expansion of M-MDSCs in patients with endometriosis compared to controls. In vitro, Pro-EGCG compromised human M-MDSC survival and impaired their suppressive capacity by inhibiting ROS, Arg-1, and NO production. Furthermore, M-MDSC-induced stromal cell proliferation and fibrotic gene expression were abolished by Pro-EGCG preconditioning.</p><p><strong>Conclusion: </strong>Pro-EGCG hinders endometriosis progression by inhibiting M-MDSC accumulation, immunosuppressive functions, and pro-endometriotic activities. These findings position Pro-EGCG as a potential immunotherapy for endometriosis and other M-MDSC-driven inflammatory disorders.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13321424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367618","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":"Jiedu Huoxue decoction inhibits cardiomyocyte apoptosis via PTEN/AKT/GSK3β-mediated mitochondrial dynamics in myocardial infarction: an integrative study of network pharmacology, transcriptomics and molecular docking.","authors":"Mingjie Pang, Han Peng, Changlei Hu, Yutong Li, Yangzhen Pei, Bin Liu, Yuting Wu, Guanghong Chen, Haozhen Cui, Aihua Shen, Li Zheng, Lingpeng Xie, Yingchun Zhou, Guoyong Zhang, Xin Han","doi":"10.1186/s13020-026-01444-7","DOIUrl":"10.1186/s13020-026-01444-7","url":null,"abstract":"<p><strong>Background: </strong>Myocardial infarction (MI) triggers oxidative stress, mitochondrial dysfunction, and cardiomyocyte apoptosis. At present, it remains urgently needed to develop novel therapies specifically suppressing cardiomyocyte apoptosis via improving mitochondrial dysfunction following MI. Jiedu Huoxue Decoction (JDHXD) may have the effect of ameliorating myocardial injury after MI.</p><p><strong>Purpose: </strong>This study examined the protection exerted by JDHXD against myocardial injury post-MI and investigated the underlying mechanisms of action.</p><p><strong>Methods: </strong>UHPLC/Orbitrap-MS, network pharmacology and transcriptome analysis were used to study the effective components and potential targets of JDHXD for treating MI. In vivo: The MI mice received JDHXD (12.74/25.48 g/kg/day) or captopril treatment for 28 days. Later, cardiac function (tested by echocardiography and histopathology), apoptosis, oxidative stress, mitochondrial ultrastructure, mitochondrial fission/fusion and PTEN/AKT/GSK3β pathway protein levels were evaluated. In vitro: TBHP-induced cardiomyocytes (H9C2 cells and NCMs) were exposed to JDHXD treatment (50-200 μg/mL), with or without PTEN inhibitor Bpv (2 μM) or PTEN overexpression (through adenoviral transduction). Afterwards, cell apoptosis, oxidative stress, mitochondrial membrane potential, and relative proteins were assayed. Experiments such as molecular docking and surface plasmon resonance imaging (SPRi) were conducted to verify the effective components of JDHXD in preventing myocardial mitochondrial injury after MI.</p><p><strong>Results: </strong>The results of network pharmacology and transcriptomics suggest that JDHXD may ameliorate myocardial injury after MI through modulating PTEN for activating the PI3K/AKT/GSK3β signaling pathway. In vivo: JDHXD dose-dependently improved left ventricular function, improved the oxidative stress-induced imbalance of mitochondrial fission/fusion, and inhibited cardiomyocyte apoptosis post-MI in association with suppressing the PTEN/AKT/GSK3β pathway. In vitro: JDHXD suppressed the TBHP-induced cardiomyocyte apoptosis, attenuated oxidative stress, preserved mitochondrial potential, and restored mitochondrial dynamics. PTEN inhibitor did not augment JDHXD's effects, whereas PTEN overexpression partially abolished JDHXD's protection against myocardial injury induced by oxidative stress. UHPLC/Orbitrap-MS, molecular docking, SPRi and experiments in vitro confirmed that puerarin is one of the main components of JDHXD in regulating the PTEN/AKT/GSK3β pathway to improve mitochondrial function after MI and inhibit cardiomyocyte apoptosis.</p><p><strong>Conclusions: </strong>JDHXD against oxidative stress-induced cardiomyocyte apoptosis post-MI through ameliorating mitochondrial dysfunction, which is partially mediated by suppressing the PTEN/AKT/GSK3β pathway to inhibit excessive mitochondrial fission and promote mitochondrial fusion.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13312624/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148350922","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":"The IL-17A modulating astrocytic activity was associated with the electroacupuncture-mediated improvement of sensorimotor ability after stroke.","authors":"Yuenming Yau, Zeli Li, Zhiyuan Jiang, Jianyu Luo, Zhennan Wu, Chang Liu, Nenggui Xu, Lulu Yao","doi":"10.1186/s13020-026-01446-5","DOIUrl":"10.1186/s13020-026-01446-5","url":null,"abstract":"<p><p>Both clinical and preclinical evidence showed that electroacupuncture (EA) at Baihui (Governing Vessel 20, GV20) and Dazhui (GV14) could relieve sensorimotor disability after ischemic stroke (IS). However, the mechanism behind this therapeutic remains to be unraveled, and the current findings of its underlying mechanism are mainly focusing on neurons, with little evidence from astrocyte. Astrocyte plays an essential role in IS pathology, and IL-17A as a critical mediator in IS. This study aimed to investigate the relationship between the activity of astrocyte and expression of IL-17A during the regulation of sensorimotor function. The sensorimotor-related behaviors in mice were assessed by using Adhesive removal test and Rotarod test, and the expression/function of IL-17A was evaluated by ELISA, RT-PCR, and Western Blot. In vivo calcium activity of astrocyte was detected by two-photon calcium imaging. Our results revealed that EA preconditioning promoted the recovery of sensorimotor function in IS mice, and this therapeutic effect was absent when the astrocytic activity was chemogenetically inhibited. In addition, astrocytic calcium activity of IS mice could be mimicked by overexpressing IL-17A. Altogether, these results suggested the IL-17A in the astrocyte may play a key role in the functional recovery after stroke. These findings not only elucidate a critical pathway for understanding how IL-17A in astrocytic calcium activity influences the functional recovery after stroke, but also suggest a potential valuable therapeutic strategy for stroke.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13312517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148350984","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-derived immunometabolic modulators: traditional Chinese medicine at the crossroads of metabolism and antitumor immunity.","authors":"Bo Zhang, Na Wang, Xiaoshan Wang, Xuerui Wang, Lihan Shang, Bingsheng Sun, Fanming Kong","doi":"10.1186/s13020-026-01448-3","DOIUrl":"10.1186/s13020-026-01448-3","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Traditional Chinese Medicine (TCM) has long been applied in oncology to \"support vital Qi and eliminate pathogenic factors\", yet its place within modern immunometabolic therapy is still not clearly defined. Tumor, stromal, and immune cells are now understood to be organized around several recurrent metabolic axes, including glycolysis-lactate, mitochondrial stress and immunogenic cell death (ICD), lipid-bile-acid signaling, and redox balance. Clarifying how herb-based formulas, isolated compounds, and contemporary delivery systems influence these axes may provide a mechanistic foundation for integrating TCM into precision cancer treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Main body: &lt;/strong&gt;This narrative review brings together ethnopharmacological knowledge with pharmacological and mechanistic studies, omics-based profiling, and emerging nanomedicine reports that examined TCM-derived interventions with defined metabolic and immune outcomes in solid tumors. We first outline how metabolic reprogramming of the tumor microenvironment (TME) shapes major immune populations, including dendritic cells (DCs), CD8⁺ T cells, tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), and NK/NKT cells. We then arrange representative herb-derived agents along four immunometabolic axes. Across Axis I-IV, multiple prescriptions and monomers have been reported to attenuate tumor glycolytic flux and lactate burden, induce mitochondrial damage and ferroptosis-linked ICD, normalize lipid-bile-acid-centered myeloid niches, and improve DC and T-cell metabolic fitness. Examples include Astragalus-based formulas, Gegen Qinlian decoction (GQD), ginsenosides, berberine, licochalcone A, emodin, celastrol-Rg3 and iron-based nanoplatforms, Jianpi Jiedu and Jianpi Huayu decoctions, Compound Kushen Injection, Compound Fuling Granule, Hochu-ekki-to, Kejinyan decoction, Huaier, Ganoderma polysaccharides, Shenqi Yiqi Capsule, and polysaccharide-loaded vesicles or microneedles. Finally, we relate these axes to classical TCM doctrines such as Fuzheng Quxie, Tiaogan Hepi, and Peiben Chuzhuo, proposing a clinically oriented, syndrome-informed framework.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;TCM-derived interventions can be systematically positioned along four convergent immunometabolic axes that coordinate interactions between tumors and the immune system. Considering TCM as an immunometabolic co-therapy highlights its potential to convert \"cold\" tumors into \"hot\" lesions, deepen responses to chemo-, radio- and immunotherapy, and, in some contexts, improve treatment tolerance. Future studies should emphasize rigorous mechanistic dissection, standardized and chemically defined formulations, biomarker-guided patient selection, and well-designed prospective clinical trials to translate this axis-based framework into precision integrative oncology. However, most TCM-derived immunometabolic interventions remain incompletely validated, and their translation ","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13308254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337995","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":"Paishi granule inhibits calcium oxalate-induced oxidative stress kidney injury after gut microbiota transformation: a multi-omics analysis combined in vivo and in vitro study.","authors":"Bingqi Zhang, Xingxu Pan, Xiaolin Xie, Shiqi Fan, Tiantian Tan, Danqi Li, Jingsong Jin, Qiushi Cao","doi":"10.1186/s13020-026-01439-4","DOIUrl":"10.1186/s13020-026-01439-4","url":null,"abstract":"<p><strong>Background: </strong>Renal stones are a common clinical problem with a high recurrence rate. In recent years, many Chinese herbs have been reported to effectively ameliorate calcium oxalate via different mechanisms. Gut microbiota plays an important role in the regulation of stone formation. In this study, we establish a novel molecular framework to illuminate that paishi granule (PSG) can treat calcium oxalate stone formation through gut microbiota transformation.</p><p><strong>Methods: </strong>The UPLC-MS/MS of serum-PSG was analyzed. A rat model of calcium oxalate kidney stones and a calcium oxalate monohydrate cell model (COM) were established. Blood samples were measured for Scr and BUN level. The histological staining and immunohistochemistry were used for observing pathological morphology of the kidneys and the colon. 16S rRNA sequencing, fecal metabonomics analysis, RNA transcriptomics sequencing, enzyme-linked immunosorbent assays, RT-qPCR, and western blotting were used to identify the signal transduction pathway of PSG in treating renal calculi to systematically explain the function of PSG after transformation by the gut microbiota.</p><p><strong>Results: </strong>PSG significantly alleviated renal injury induced by calcium oxalate stones, reduced BUN and Scr levels, and exerted antioxidant effects by enhancing T-SOD activity while decreasing LDH and MDA levels. Histological analysis of intestinal tissues demonstrated that PSG repaired intestinal barrier damage in EN rats. 16S rRNA sequencing revealed a decrease in the abundance of genera such as Romboutsia, Clostridium, and Enterobacter, and an increase in that of Blautia, Acetatifactor, and Kineothrix in EN group. SCFAs metabonomics analysis indicated significant reductions in acetate, propionate, and butyrate levels, which were improved after treatment with PSG, effectively ameliorating the disordered microbiota structure and metabolite profiles. The key differentially expressed genes, including β-arrestin2, TGF-β1, and NOX4, were identified using transcriptomics analysis, and enrichment analysis suggested the involvement of the MAPK signaling pathway. RT-qPCR and western blotting confirmed that PSG mitigated oxidative stress by suppressing the β-arrestin2/MAPK/NOX4 pathway. The renal protective effects of PSG were markedly attenuated in an antibiotic-induced model of gut-microbiota depletion. In vitro experiments further demonstrated that the PSG, after being transformed by the microbiota, could regulate the MAPK kinase cascade reaction through the mechanism mediated by β-arrestin2, inhibiting the process of NOX4 expression.</p><p><strong>Conclusion: </strong>PSG exerts its anti-lithic effects through a novel multi-target regulatory mechanism involving the gut microbiota-metabolite-oxidative stress axis, thereby establishing a new paradigm for mechanistic research in traditional Chinese medicine.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13295731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148327028","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":"Panax quinquefolium saponin decreases atherosclerosis in ovariectomized ApoE^-/- mice via regulating estrogen receptor α.","authors":"Li Chen, Jun-He Shi, Xiao-Juan Ma, Hua Chai, Kang-Kang Wei, Zhen Yang, Yu Tan, Hong-Bo Huang, Da-Zhuo Shi, Hua Qu","doi":"10.1186/s13020-026-01410-3","DOIUrl":"10.1186/s13020-026-01410-3","url":null,"abstract":"<p><strong>Background: </strong>Postmenopausal women are at an increased risk for atherogenesis. Panax quinquefolium saponin (PQS) has demonstrated beneficial effects on decreasing inflammatory response, alleviating oxidative stress and improving endothelial function. However, the effect of PQS on atherogenesis in postmenopausal women remains unknown. This study explored the effects of PQS on different pathological stages (8 or 14 weeks) of atherogenesis in ApoE^-/- mice with mimicking postmenopausal condition by ovariectomy.</p><p><strong>Methods: </strong>Atherosclerotic plaque, levels of serum inflammatory cytokines and apoptosis of aortic endothelium were detected. Human umbilical vein endothelial cells (HUVECs) treated with oxidized low-density lipoprotein (ox-LDL) were used to investigate the mechanism. Using network pharmacology, molecular docking and receptor inhibitor to explore the target of PQS in ovariectomized ApoE^-/- mice.</p><p><strong>Results: </strong>ApoE^-/- mice subjected to ovariectomy displayed an increase in atherosclerotic plaque formation, levels of serum inflammatory cytokines and apoptosis of aortic endothelial cells. PQS treatment counteracted these detrimental effects both at 8 and 14 weeks. Network pharmacology and molecular docking analysis revealed that PQS targeted estrogen receptor α (ERα) in ovariectomized ApoE^-/- mice, a key regulator in inflammation and aortic endothelial apoptosis. PQS regulated inflammation and apoptosis via ERα/PI3K/Akt and ERα/MEK/ERK1/2 pathways. ERα inhibitor mostly counteracted the beneficial effects of PQS on ovariectomized ApoE^-/- mice and injured HUVECs, in contrast, ERα activator enhanced these effects.</p><p><strong>Conclusions: </strong>The study indicated that PQS decreased atherosclerotic plaque by reducing inflammation and apoptosis of aortic endothelium in ovariectomized ApoE^-/- mice via regulating ERα, providing new insights into PQS as a therapeutic target in postmenopausal atherosclerosis.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13285194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293608","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}