Chinese Medicine最新文献

{"title":"Renqing Mangjue modulates chronic atrophic gastritis inflammation-cancer transition via the cGMP-PKG/PI3K-AKT pathway.","authors":"Fengyu Huang, Peiping Chen, Daiyue Ding, Changyue Song, Xiangying Kong, Haiping Wang, Hua Zhou, Tao Su, Na Lin, Xiaohui Su","doi":"10.1186/s13020-026-01457-2","DOIUrl":"10.1186/s13020-026-01457-2","url":null,"abstract":"<p><strong>Background: </strong>Chronic atrophic gastritis (CAG) is a critical stage in the progression from inflammation to cancer and is closely associated with an increased risk of gastric cancer (GC). Renqing Mangjue (RQMJ), a traditional Tibetan herbal remedy, has shown diverse pharmacological properties, including regulation of gastrointestinal function and anti-inflammatory effects. However, the specific effects and mechanisms by which RQMJ influences the transition from inflammation to cancer remain unclear.</p><p><strong>Objectives: </strong>This study aimed to evaluate the preventive and therapeutic effects of RQMJ on CAG and its intervention in the inflammation-cancer transition process, with a focus on exploring the underlying molecular mechanisms.</p><p><strong>Methods: </strong>RQMJ was chemically characterized by UPLC-Q-TOF-MS/MS and HPLC. A rat model of CAG and its inflammation-cancer transition was established and treated with different doses of RQMJ. The therapeutic effects of RQMJ were evaluated by gross gastric mucosal observation, ELISA, histopathological staining, immunohistochemistry, and Western blot analysis. In vitro, the effects of RQMJ on inflammation and migration of the gastric precancerous cell model (MC cells) were assessed using ELISA, wound-healing, Transwell migration, and Western blot assays. RNA sequencing and molecular biology techniques were then employed to explore the underlying mechanisms, and key targets were further validated in both in vivo and in vitro experiments. Finally, C-type natriuretic peptide (CNP) was used to verify the involvement of the identified signaling pathway.</p><p><strong>Results: </strong>A total of 2780 chemical constituents were identified in RQMJ. A dynamic rat model of CAG and its progression to GC was established. During CAG, persistent inflammation and aberrant PI3K-AKT activation formed a positive-feedback loop, driving FAK overexpression and epithelial-mesenchymal transition (EMT)-related changes, which remained active in GC despite partial reduction of inflammation. RQMJ markedly alleviated gastric mucosal injury, suppressed intestinal metaplasia, and improved gastrointestinal function. It also reduced pro-inflammatory mediators (TNF-α, IL-1β, CRP), increased IL-10, and downregulated tumor-related markers (Ki-67, Vimentin, CA19-9). In vitro, RQMJ inhibited MC cell proliferation and migration, suppressed inflammatory and EMT-related proteins. Mechanistically, RQMJ activated the cGMP-PKG pathway and inhibited the PI3K-AKT signaling pathway, thereby disrupting inflammatory amplification. This further downregulated extracellular matrix (ECM)-receptor interaction molecules (TGF-β, FAK, Itga2), ultimately blocking the inflammation-cancer transition.</p><p><strong>Conclusion: </strong>RQMJ may activate the cGMP-PKG signaling pathway while suppressing aberrant PI3K-AKT activation, thereby reducing inflammatory cytokine levels and inhibiting ECM remodeling and the EMT-associated pr","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13366807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444738","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":"Natural polysaccharides targeting mitochondrial function for colorectal cancer prevention and treatment: mechanisms and nano-delivery strategies.","authors":"Huan Yan, Lianfeng Wang, Jiaxin Gan, Xin Zhou, Yuxin Jiang, Honglian Wang, Yuting Luo, Juan Fu, Jianqin Liu, Zhi Li","doi":"10.1186/s13020-026-01463-4","DOIUrl":"10.1186/s13020-026-01463-4","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is a malignant tumor of the digestive system with high incidence and mortality worldwide. Mitochondrial dysfunction plays a central role in the development, progression, and chemotherapy resistance of CRC. Natural polysaccharides have attracted increasing attention in anti-CRC research in recent years due to their wide sources, low toxicity, good biocompatibility, and multi-target activities.</p><p><strong>Objective: </strong>To systematically review the molecular mechanisms by which natural polysaccharides target mitochondrial dysfunction to prevent and treat CRC, and to summarize the research progress of nano-delivery strategies.</p><p><strong>Methods: </strong>A systematic search was conducted in PubMed, Web of Science, Scopus, and SinoMed databases for literature published from January 1, 2015 to June 3, 2026. A total of 89 articles were included for analysis.</p><p><strong>Results: </strong>Natural polysaccharides exert anti-CRC effects through synergistic actions of multiple pathways, including regulation of reactive oxygen species homeostasis, induction of mitochondrial apoptosis and autophagy, remodeling of the tumor immune microenvironment, and protection of intestinal barrier function. Their bioactivities are closely related to molecular weight, monosaccharide composition, glycosidic bond type, branching structure, and chemical modification. Nano-delivery technologies can significantly improve their targeting efficiency and therapeutic activity. Regarding clinical studies, current evidence mainly focuses on the combined use of natural polysaccharides with chemotherapy and the management of cancer-related symptoms; direct clinical evidence targeting CRC resistance remains limited.</p><p><strong>Conclusion: </strong>Mitochondria-targeting nano-systems based on natural polysaccharides provide a promising multi-target strategy for CRC prevention, treatment, and reversal of chemotherapy resistance. However, current evidence has limitations, including inconsistent structural characterization, lack of direct co-localization evidence, and insufficient pharmacokinetic-pharmacodynamic evaluations.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13366997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444748","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":"Beyond transparency: why Traditional Chinese Medicine (TCM) need explainable artificial intelligence (XAI).","authors":"Wanting Zheng, Yuanyuan Tong, Jinjian Huang, Ling Zhu, Jiaqi Chai","doi":"10.1186/s13020-026-01455-4","DOIUrl":"10.1186/s13020-026-01455-4","url":null,"abstract":"<p><p>The integration of artificial intelligence (AI) with Traditional Chinese Medicine (TCM) is rapidly expanding, creating new opportunities for digital diagnosis, syndrome differentiation, prescription recommendation, multimodal clinical support, and knowledge mining. The central obstacle to this integration, however, lies beyond predictive performance and stems from a fundamental epistemological mismatch between data-driven AI and theory-driven TCM. Contemporary AI systems often operate through opaque statistical representations, whereas TCM depends on holistic, relational, and interpretive reasoning centered on syndrome differentiation and disease-mechanism inference. Consequently, explainable artificial intelligence (XAI) is required not merely to improve transparency but to serve as an epistemic interface that enables semantic translation between machine-discovered patterns and TCM clinical reasoning. This review argues that AI-TCM integration should be understood as an epistemological integration problem rather than a purely technical one. To address this problem, we introduce two conceptual lenses: the dual-layer opacity framework, which captures the superposition of algorithmic opacity and the theoretical opacity of TCM knowledge, and the semantic translation framework, which conceptualizes XAI as the process of mapping computational features and reasoning traces onto clinically meaningful and theory-consistent TCM concepts. On this basis, we critically synthesize major methodological pathways of TCM-XAI, including feature-attribution methods, visual explanation, intrinsically interpretable models, knowledge-guided reasoning, and large-language-model-based explanation infrastructures such as chain-of-thought and graph-based retrieval-augmented generation. Beyond methodological synthesis, we identify four core criteria for high-quality explanation in TCM: faithfulness, clinical relevance, theoretical coherence, and cultural integrity. We show that the principal challenges of TCM-XAI extend beyond accuracy and include annotation uncertainty, explanation validation, privacy-preserving interpretability, fairness across populations, and the risk of epistemic reduction or cultural misinterpretation. Finally, we outline a future research agenda centered on causal inference, neuro-symbolic reasoning, multimodal explanation benchmarks, clinician-centered evaluation, and regulatory standards for trustworthy TCM-AI systems. We argue that XAI should be understood not as a technical add-on but as the epistemic infrastructure required to build clinically trustworthy, culturally coherent, and scientifically robust AI ecosystems for Traditional Chinese Medicine.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13366969/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444806","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":"Rhein from a traditional herbal formula attenuates hepatic fibrosis via ALDH1A3-mediated retinoic acid metabolism.","authors":"Kai Yu, Minqi Chen, Wanchao Hou, Jinhua Lu, Qianhan Liu, Wanrong Zeng, Yan Xie, Zhengcai Du, Xiaotao Hou, Erwei Hao, Jiagang Deng","doi":"10.1186/s13020-026-01465-2","DOIUrl":"10.1186/s13020-026-01465-2","url":null,"abstract":"<p><strong>Background: </strong>Hepatic fibrosis is a prevalent outcome of chronic liver diseases. Although activation of hepatic stellate cell (HSC) is a primary driver of fibrogenesis, therapeutic strategies targeting retinoic acid (RA) metabolism in HSCs remain insufficiently investigated. This study aimed to elucidate the material basis of Huanggen formula (FHG), identify its principal bioactive constituents, and clarify the underlying antifibrotic mechanisms.</p><p><strong>Method: </strong>The antifibrotic efficacy of FHG was assessed in a CCl₄-induced mouse model. Widely-targeted and untargeted metabolomics were conducted to characterize FHG constituents and serum-absorbed components, followed by high-content screening to evaluate anti-HSC activation activity. Rhein was further examined in TGF-β1-stimulated LX-2 cells and CCl₄-induced mice. Label-free proteomics, multiple reaction monitoring quantification, DARTS, CETSA, and molecular docking were performed to identify the molecular targets of rhein. ALDH1A3 inhibition, knockdown, and overexpression were employed to verify its functional role in LX-2 cells.</p><p><strong>Results: </strong>FHG markedly alleviated metabolic disturbances and histopathological injury in fibrotic mice. Metabolomic analysis identified anthraquinones and flavonoids as the principal active classes, with rhein exhibiting potent anti-HSC activation effects. Rhein suppressed LX-2 activation, extracellular matrix (ECM) accumulation, and migration, and mitigated CCl₄-induced hepatic fibrosis. Proteomic analysis indicated that rhein regulated ECM remodeling, mitochondrial function, and RA metabolism, accompanied by significant upregulation of DHRS4 and ALDH1A3. Mechanistically, rhein directly targeted to ALDH1A3, enhanced its expression, and increased intracellular ATRA level. The inhibition of ALDH1A3 partially abrogated the effects of rhein. Knockdown and overexpression experiments verify that ALDH1A3 is a critical negative regulator of HSC activation.</p><p><strong>Conclusion: </strong>Rhein is a key antifibrotic constituent of FHG and suppresses hepatic fibrosis by targeting ALDH1A3 and restoring RA metabolism. The ALDH1A3-ATRA axis represents a central mechanism and a promising therapeutic target.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13366891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444779","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":"Electroacupuncture enhances anti-tumor immunity in TNBC by reducing NE release and blocking α2-AR-mediated NGF/Hippo signaling.","authors":"Fei-Fei Li, Yan Huang, Chun-Fang Gao, Chun-Yu Wu, Chen-Ping Sun, Yue-Nong Qin, Ying Xie, Sheng Liu, Huan-Gan Wu","doi":"10.1186/s13020-026-01445-6","DOIUrl":"10.1186/s13020-026-01445-6","url":null,"abstract":"<p><strong>Background: </strong>Targeting the neuro-immune microenvironment to suppress triple-negative breast cancer (TNBC) represents a critical strategy in tumor immunotherapy.</p><p><strong>Methods: </strong>A syngeneic 4T1 orthotopic TNBC model in Balb/c mice was employed. EA was applied at ST36 (Zusanli) using systematically optimized parameters (2/15 Hz, 3 mA, 30 min, every other day). Multi-dimensional immunophenotyping by flow cytometry, immunofluorescence, and Western blot was performed across tumor, blood, and splenic compartments. Transcriptome sequencing coupled with KEGG/GSEA pathway analysis was used to identify downstream signaling networks. The NGF/Hippo/YAP axis and adrenergic receptor subtype specificity were validated through pharmacological intervention in vitro, while EA synergy with αPD-L1 was assessed in a CD8⁺ T cell-depletion model.</p><p><strong>Results: </strong>ST36 stimulation at 3 mA preferentially suppressed TNBC tumor growth and augmented intratumoral immune infiltration, characterized by elevated CD8⁺ T cells, NK cells, and M1-polarized macrophages. EA significantly enhanced CD8⁺ T cell effector capacity, upregulating perforin, granzyme B, CD69, and ZAP70 phosphorylation, and synergized with αPD-L1 in a CD8⁺ T cell-dependent manner. Mechanistically, EA activated c-Fos⁺/ChAT⁺ cholinergic neurons in the dorsal motor nucleus of the vagus (DMV) and reduced norepinephrine (NE) output in both circulation and tumors. Transcriptomic profiling identified NGF downregulation and Hippo pathway activation as central events. EA upregulated AMOT, driving YAP phosphorylation at Ser127, cytoplasmic sequestration of YAP, and suppression of downstream IL-6 secretion. In vitro, exogenous NGF suppressed YAP phosphorylation and promoted TNBC malignant behavior, effects fully reversed by the YAP inhibitor verteporfin. α2-adrenergic receptor (α2-AR) antagonism with yohimbine abrogated NE-induced NGF upregulation, pinpointing α2-AR as the receptor subtype linking sympathetic signaling to the NGF/Hippo axis.</p><p><strong>Conclusion: </strong>EA at ST36 recalibrates neuro-sympathetic tone in TNBC by activating vagal cholinergic outflow, reducing NE-driven α2-AR/NGF/Hippo signaling, and thereby relieving immunosuppression while amplifying CD8⁺ T cell-mediated cytotoxicity. These findings establish a neuro-immune mechanistic framework for EA-based adjuvant immunotherapy in TNBC.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13361121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148434924","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":"Qishen Granules attenuate adverse ventricular remodeling in chronic heart failure by promoting Legumain/Arg1/Rac1-mediated efferocytosis of resident cardiac macrophages.","authors":"Meijiao Tao, Shixuan Min, Jiali Liu, Huishi Xiao, Tong Xiao, Sisi Liang, Xin Liu, Jun Wang, Yulin Ouyang, Ruijia Wen, Lei Wang, Wei Wang, Yao Zhang, Chun Li","doi":"10.1186/s13020-026-01461-6","DOIUrl":"10.1186/s13020-026-01461-6","url":null,"abstract":"<p><strong>Background: </strong>Ventricular remodeling is a key pathological feature of chronic heart failure (CHF). Following myocardial infarction (MI), impaired macrophage efferocytosis sustains cardiac inflammation, disrupts tissue repair, and accelerates adverse remodeling and dysfunction. Qishen Granules (QSG) is a classical traditional Chinese medicine formulation used in the clinical treatment of heart failure. However, its regulatory effects on efferocytosis in resident cardiac macrophages (RCMs) remain unclear.</p><p><strong>Purpose: </strong>This study aimed to elucidate the molecular mechanisms by which QSG regulates Legumain-mediated efferocytosis in RCMs and to identify the key bioactive compounds.</p><p><strong>Methods: </strong>A mouse model of post-MI heart failure was established via ligation of the left anterior descending coronary artery. The therapeutic effects of QSG were evaluated in isolated RCMs obtained using magnetic-activated cell sorting. Mechanistic investigations were conducted using transcriptomic analysis, network pharmacology, live-cell imaging, and siRNA-mediated gene silencing. In addition, UPLC-Q-Exactive MS, molecular docking, and molecular dynamics simulations were employed to systematically study the active compounds of QSG.</p><p><strong>Results: </strong>QSG treatment restored the population of RCMs and enhanced their efferocytic capacity in CHF, thereby reducing cardiomyocyte apoptosis, promoting inflammatory resolution, and improving ventricular structure and function. Mechanistically, QSG upregulated Legumain expression and activated the Arg1/Rac1 signaling axis to facilitate cytoskeletal remodeling and enhance phagocytic efficiency. Further analyses identified tanshinone IIA, neocryptotanshinone and calycosin as the core bioactive compounds of QSG. All three compounds upregulated Legumain expression and exhibited stable binding affinity toward Legumain.</p><p><strong>Conclusion: </strong>QSG restores efferocytic capacity in RCMs by targeting the Legumain/Arg1/Rac1 signaling axis, thereby attenuating adverse ventricular remodeling in CHF.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410543","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":"Resveratrol-activated PI3K/AKT/mTOR signaling pathway attenuates ferroptosis by promoting NRF2/GPX4 metabolic pathway to mitigate IFN-gamma-mediated aplastic anemia.","authors":"Erhao Zhang, Jianan Cui, Xinran Zhu, Juan Chen, Liqin Xu, Xiaomin Li, Yufei Zhang, Hui Jia, Xiaorong Zhou, Zenghua Lin, Han Wang, Hong Liu","doi":"10.1186/s13020-026-01462-5","DOIUrl":"10.1186/s13020-026-01462-5","url":null,"abstract":"<p><strong>Background: </strong>Aplastic anemia (AA) is a severe hematological disorder caused by hyperactivated T cell-mediated hematopoietic failure. It is characterized by hematopoietic stem cell deficiency and hypocellular hematopoiesis in the bone marrow (BM). Ferroptosis, a specific type of programmed cell death, is defined by iron-dependent lipid peroxidation, which has garnered the attention of researchers due to its unique role and biological importance in various diseases. However, the correlation between immunological imbalance-induced ferroptosis and the mortality of hematopoietic stem cells within the BM microenvironment in AA is unclear. Resveratrol (RSV) is crucial in activating NRF2, hence influencing the onset and progression of diseases by regulating ferroptosis. This study aimed to investigate the roles and molecular mechanisms of RSV in the hematopoietic recovery of AA regarding ferroptosis.</p><p><strong>Methods: </strong>We measured some biomarkers in AA mice and IFN-gamma-treated 32D cells, representing AA syndromes and ferroptosis features. Furthermore, in RSV-treated 32D AA cells, cell activity, cell apoptosis, mitochondrial membrane potential, mitochondrial membrane permeability, and intracellular levels of MDA, ferrous iron, 4-HNE, GSH, ROS, and lipid peroxidation were assessed. Subsequently, additional in vitro and in vivo experiments were performed to investigate the mechanisms by which RSV effectively regulates NRF2 stability, further inhibiting ferroptosis in AA.</p><p><strong>Results: </strong>We demonstrated that ferroptosis contributes to the occurrence and development of AA disease. RSV dose-dependently inhibits ferroptosis in 32D AA cells by targeting GPX4 expression, enhancing the cell activity of hematopoietic BM cells. Mechanically, RSV significantly increases NRF2 phosphorylation through the PI3K/AKT/mTOR signaling pathway, which maintains NRF2 stability to promote the GPX4 metabolic pathway in AA. Protein levels of p-AKT, p-mTOR, p-NRF2, and GPX4 were markedly increased in BM cells in RSV-treated AA mice, resulting in the suppression of AA development.</p><p><strong>Conclusion: </strong>Our data demonstrate that RSV effectively inhibits ferroptosis in AA or IFN-gamma-treated 32D cells by targeting the PI3K/AKT/mTOR signaling pathway, which enhances NRF2-mediated GPX4 transcription, thereby ameliorating AA symptoms in vitro and in vivo. This study concludes that RSV is a potential therapeutic drug for ferroptosis-related AA treatment.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410591","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":"Xifeng Zhichou decoction mitigates tic disorder on juvenile rats by regulating neuroinflammation and neurotransmitter homeostasis: dual modulation of Nr4a2 and gut microbiota.","authors":"Ruolan Wu, Jinlan Peng, Mingyue Zhang, Qing He, Jin Luo, Qinqiang Long, Xue Xiao, Shasha Li, Lisheng Wan","doi":"10.1186/s13020-026-01464-3","DOIUrl":"10.1186/s13020-026-01464-3","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Xifeng Zhichou decoction (XFZCD), a modified formulation of Chinese medicine, demonstrates significant clinical efficacy in treatment of tic disorder (TD). However, its efficacy and therapeutic mechanisms remain insufficiently characterized.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;This study aims to comprehensively evaluate the anti-TD effect of XFZCD in a rat model, and to elucidate the underlying mechanism.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Ultra-performance liquid chromatography-mass spectrometry (UPLC-MS) was used to quality analyze of XFZCD, while network pharmacology was employed to predict core compounds and potential mechanisms. A juvenile TD rat model was established via intraperitoneal injection of 3,3-iminodipropionitrile, and the therapeutic effects of XFZCD were evaluated using behavioral tests, cytokine assays, and immunohistochemistry. Transcriptomics and 16S rRNA sequencing were employed to elucidate the mechanisms by investigating regulatory gene and gut-brain axis. Western blot (WB) and enzyme-linked immunosorbent assay were utilized to focus and verify the potential mechanisms. Untargeted metabolomics was conducted to confirm the crucial pathway from the perspective of terminal metabolites. Furthermore, Nr4a-targeted siRNA knockdown in Lipopolysaccharides (LPS)-challenged SH-SY5Y cells was performed to verify the core regulatory role of Nr4a2 in XFZCD-mediated neuroprotection.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The UPLC-MS analysis identified 66 compounds in XFZCD. Network pharmacology highlighted serotonergic and dopaminergic synapses, and JAK-STAT signaling in enrichment analysis, suggesting XFZCD treats TD by regulating neuroinflammation and neurotransmitter homeostasis. XFZCD significantly mitigated tics, abnormal motor behavior, and anorexia in rat models, while also attenuating striatal neuroinflammation and oxidative stress, thereby exhibiting a substantial therapeutic effect on TD. Transcriptomic analysis identified Nr4a2 as a pivotal regulatory gene, which exhibited strong binding affinity with the core components identified via network pharmacology. 16S rRNA sequencing revealed that XFZCD modulated intestinal function by restoring the Firmicutes/Bacteroidetes ratio. WB and ELISA experiments confirmed that XFZCD could suppress inflammatory responses and restore central neurotransmitter homeostasis. Untargeted metabolomics indicated XFZCD reversed TD-caused abnormal bile acid metabolism, which was closely correlated with gut microbial remodeling. Cellular experiments confirmed that Nr4a2 silencing largely abrogated XFZCD's inhibitory effects on neuroinflammation and its regulatory function on neurotransmitter balance.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;XFZCD demonstrates significant efficacy in the treatment of TD by inhibiting inflammation and balancing neurotransmitters through dual modulation of Nr4a2 and intestinal flora. Notably, the regulation of Nr4a2 and bile acid metabolism emerges as a pro","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410587","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":"Advances in electroacupuncture for perioperative neurocognitive disorders: mechanisms and clinical evidence.","authors":"Shirong Wei, Sitong Zhou, Junwen Tu, Tong Zhi, Yungong Wang, Qihong Shen, Chaobo Ni, Ming Yao, Huadong Ni","doi":"10.1186/s13020-026-01466-1","DOIUrl":"10.1186/s13020-026-01466-1","url":null,"abstract":"<p><p>Perioperative neurocognitive disorders (PND), including postoperative delirium, delayed neurocognitive recovery, and postoperative cognitive dysfunction, are common complications in older surgical patients and are associated with impaired recovery, reduced quality of life, and increased postoperative morbidity. Current management remains largely supportive and preventive, and effective targeted therapies are still lacking. Electroacupuncture (EA), as a minimally invasive neuromodulatory intervention, has attracted increasing attention because of its potential multi-target regulatory effects. This review summarizes current mechanistic and clinical evidence regarding EA for PND. Preclinical studies suggest that EA may modulate several interacting pathological processes, including neuroinflammation, oxidative stress, autophagy dysfunction, ferroptosis, mitochondrial injury, microbiota-gut-brain axis dysregulation, and hippocampal synaptic plasticity. Recent PND/POCD animal studies further support EA-related regulation of NLRP3 inflammasome activation, cGAS-STING signaling, SIRT1/NRF2/GPX4-mediated ferroptosis, AMPK/SIRT1/FOXO1/PINK1/Parkin-related autophagy pathways, and MAPK-related synaptic plasticity. Clinical studies and meta-analyses suggest that EA and related acupoint-based electrical stimulation techniques may reduce early postoperative cognitive decline and improve short-term cognitive outcomes in older surgical patients. However, the overall evidence remains limited by heterogeneous stimulation protocols, variable acupoint prescriptions, incomplete blinding, short follow-up, and reliance on cognitive screening scales. Several proposed mechanisms are still partly inferred from non-PND models. Future studies should use standardized EA protocols, clinically relevant PND models, dynamic mechanistic assessments, and adequately powered sham-controlled trials to clarify the therapeutic role of EA in PND.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"21 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410548","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":"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}