The American journal of Chinese medicine最新文献

{"title":"Triptolide Improves Rheumatoid Arthritis by Regulating M1/M2 Balance Through the miR-223/CREBZF Axis.","authors":"Xiao-Bao Liu, Ying-Xing Xiang, Jia-Hao Yang, Fang-Shu Zou, Mei-Feng Shi, Xue-Qing Chen, Chang-Song Lin, Qiang Xu, Min-Ying Liu","doi":"10.1142/S0192415X26500734","DOIUrl":"10.1142/S0192415X26500734","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation and progressive joint damage. This study investigated the role of microRNA-223 (miR-223) in RA and evaluated the therapeutic effects of triptolide (Tri), a diterpenoid epoxide derived from the traditional Chinese medicinal herb <i>Tripterygium wilfordii</i>. A collagen-induced arthritis (CIA) mouse model was used to assess the effects of Tri and methotrexate (MTX). Micro-computed tomography, histological staining, enzyme-linked immunosorbent assay, flow cytometry, RT-qPCR, and western blot analysis were used to evaluate joint damage, inflammation, cytokine profiles, miR-223 expression, and the function of CREBZF, a downstream target of miR-223. CIA mice exhibited marked joint inflammation, swelling, bone erosion, and inflammatory cell infiltration, increased pro-inflammatory cytokine levels, and elevated miR-223 expression. Tri and MTX ameliorated these abnormalities and protected against bone erosion and inflammation. Tri suppressed the disease-associated elevation of miR-223, attenuated pathological fibroblast-like synoviocyte (RA-FLS) phenotypes, and shifted cytokine profiles toward an anti-inflammatory state. Dual-luciferase reporter and AGO2-RIP-qPCR assays supported direct regulation of CREBZF by miR-223. Tri restored CREBZF expression and inhibited NF-κ B signaling, thereby reducing RA-FLS proliferation and promoting apoptosis. These findings indicate that Tri ameliorates RA, at least partly, through the miR-223/CREBZF axis and identify this pathway as a potential therapeutic target.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1955-1977"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of Ferroptosis: A Novel Mechanism of Traditional Chinese Medicine in Managing Chronic Atrophic Gastritis.","authors":"Hengwang Gu, Yanzhu Chen, Yuyu Lin, Fang Wang, Binfang Zeng","doi":"10.1142/S0192415X26500394","DOIUrl":"https://doi.org/10.1142/S0192415X26500394","url":null,"abstract":"<p><p>Chronic atrophic gastritis (CAG) is a major precancerous lesion of gastric cancer, characterized by a high incidence rate, a protracted clinical course, and a well-documented risk of malignant transformation. Current Western medical treatments exert limited efficacy in reversing progressive gastric mucosal damage. In traditional Chinese medicine (TCM), CAG is categorized as expressing symptoms such as \"stomachache\" and \"abdominal fullness,\" with the core pathogenesis defined as \"spleen-stomach deficiency as the root, and qi stagnation, blood stasis, and damp-heat as the superficial manifestations.\" TCM confers distinct clinical advantages through therapeutic strategies which include invigorating the spleen and replenishing qi, clearing heat and resolving dampness, and promoting blood circulation to remove stasis. Ferroptosis, an iron-dependent form of regulated cell death, has been increasingly recognized as a key driver of gastric mucosal injury and disease progression in CAG, and exerts its effects via nine core pathways including iron metabolism imbalance, glutathione (GSH) depletion, lipid peroxidation (LPO), mitochondrial dysfunction, and inflammatory responses. This review systematically elaborates on the molecular mechanisms of ferroptosis in CAG pathogenesis and comprehensively summarizes recent advances in how active ingredients derived from Chinese herbal medicines (such as baicalein, curcumin, tanshinone IIA, astragaloside IV) and classic compound formulas like Sijunzi Decoction, Banxia Xiexin Decoction, Moluodan, and Weifuchun regulate ferroptosis-related signaling pathways. It further highlights the multi-target, multi-pathway characteristics of TCM in alleviating oxidative damage and promoting mucosal repair. Ultimately, this review aims to elucidate the scientific basis of TCM-mediated ferroptosis regulation in CAG management, provide novel theoretical support for clinical practice, and guide future directions for drug research and development.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"54 4","pages":"1061-1083"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148348019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Panax notoginseng</i> Saponins Attenuate Cerebral Ischemia-Reperfusion Injury by Suppressing Neutrophil Extracellular Traps and Ferroptosis in Brain Microvascular Endothelial Cells.","authors":"Qian Xiao, Xin-Quan Deng, Biao Tang","doi":"10.1142/S0192415X26500679","DOIUrl":"10.1142/S0192415X26500679","url":null,"abstract":"<p><p><i>Panax notoginseng</i> saponins (PNS), the chief saponin components of the traditional Chinese medicine <i>Panax notoginseng</i>, are known to ameliorate the outcomes of ischemic stroke (IS), primarily by mitigating inflammatory responses, enhancing microcirculation, and modulating oxidative stress. Damage to brain microvascular endothelial cells (BMECs) and BMECs' ferroptosis are critical steps in cerebral ischemia-reperfusion injury (CIRI), a process in which neutrophil extracellular traps (NETs) have been shown to induce BMECs injury, thereby aggravating CIRI. We aimed to investigate the regulatory effects of PNS on NETs and BMECs' ferroptosis following CIRI and evaluate its therapeutic efficacy in brain injury intervention. In this study, Sprague-Dawley rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R), and the BMECs were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R). These models were pretreated with PNS or the NETs-degrading agent DNase I, and the ensuing changes in key proteins, NETs-related markers, inflammatory factors, and ferroptosis-related indicators were assessed using Western Blotting or specific assay kits. Finally, neurological injury was assessed by neurological function scores and triphenyl tetrazolium chloride staining, while cell viability was evaluated using the Cell Counting Kit-8 (CCK-8) assay. In the rat models, PNS and DNase I markedly reduced the levels of key NETs biomarkers, related inflammatory factors, as well as MCAO/R-triggered ferroptosis, thereby mitigating brain injury. PNS treatment effectively suppressed NETs-induced ferroptosis in BMECs <i>in vitro</i>, thereby alleviating cell injury. This study demonstrated that PNS alleviates CIRI by inhibiting NETs and BMECs' ferroptosis. Mechanistically, PNS suppresses NETs, thereby suppressing ferroptosis. Collectively, these findings support a pharmacological rationale underlying the clinical treatment of IS.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1807-1821"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artemisinin Attenuates Aβ1-42 Aggregation via the CaMK IV/PKA-CREB-Ace-H4 Cascade in Neuronal Cultures and 3xTg-AD Models.","authors":"Yitian Chen, Lijun Ge, Philip Lazarovici, Wenhua Zheng","doi":"10.1142/S0192415X26500667","DOIUrl":"10.1142/S0192415X26500667","url":null,"abstract":"<p><p>Alzheimer's disease (AD), a progressive neurodegenerative disease with a rising global prevalence, is characterized by amyloid-β (Aβ) aggregation, tau hyperphosphorylation, inflammation, oxidative damage, and neuronal apoptosis. Studies have increasingly recognized epigenetic modifications as key regulators in the development of AD. Epigenetic modifications, particularly histone acetylation, are increasingly recognized as critical regulators of cell survival and AD pathogenesis. Although artemisinin (ART) exhibits potent anti-oxidative, anti-inflammatory, and neuroprotective properties, its impact on histone acetylation in AD remains uncharacterized. This study investigated whether ART regulates histone acetylation to confer neuroprotection and rescue behavioral deficits in Alzheimer's disease models. Using SH-SY5Y cells, primary neurons, and 3xTg-AD mice, we found that ART restores histone acetylation homeostasis by enhancing histone H4 acetylation. Mechanistically, this effect is driven by the activation of the CaMK IV/PKA-CREB signaling cascade. Treatment with ART reduced ROS, improved mitochondrial function, decreased Aβ1-42 deposition, and suppressed neuronal apoptosis. However, these beneficial effects were abolished by PKA or CaMK IV inhibitors. Consequently, ART treatment significantly reduced reactive oxygen species (ROS) generation, restored mitochondrial function, decreased Aβ1-42 deposition, suppressed neuronal apoptosis, and alleviated AD-like neuropathology and cognitive deficits. Crucially, the neuroprotective and epigenetic benefits of ART were entirely abolished by pharmacological inhibitors of PKA or CaMK IV. This study is the first to demonstrate that artemisinin ameliorates AD pathology and behavioral impairments via the CaMK IV/PKA-CREB-Ace-H4 axis, establishing ART as a promising therapeutic candidate for epigenetic intervention in AD.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1783-1805"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tanshinone IIA Alleviates Pyroptosis through SIRT1/NLRP3 Pathway to Improve Diabetic Nephropathy.","authors":"Wencong Tian, Peng Song, Junhao Zang, Jia Zhao, Chuntao Wang, Yanhong Liu, Hong Fang, Hongzhi Wang, Xiaojie Tian, Jiawei Zhang, Ziang Chen, Yang Gao, Yongjie Zhao, Lei Cao","doi":"10.1142/S0192415X26500102","DOIUrl":"10.1142/S0192415X26500102","url":null,"abstract":"<p><p>Diabetic nephropathy (DN) is a serious complication of diabetes mellitus, and the efficacy of standard clinical therapies is presently limited. Evidence has shown that pyroptosis-mediated cell death promotes several diabetic complications including DN. Tanshinone IIA (Tan IIA), the main fat-soluble component of <i>S. miltiorrhiza</i> Bunge, possesses anti-inflammatory and anti-oxidant properties. However, its impact on pyroptosis in DN progression and the underlying molecular mechanisms remain unclear. The aim of this study was to investigate the effect of Tan IIA on pyroptosis in DN. To establish a DN mouse model, STZ was administered to the mice for five consecutive days via injection. The mice in the treatment group then received Tan IIA by gavage for 10 weeks. Our data revealed that Tan IIA inhibited caspase-1 and gasdermin D (GSDMD)-mediated pyroptosis and thereby alleviated renal injury. Compared with that of the DN mice or high glucose-evoked HK-2 cells, the silent information regulator 1 (SIRT1) expression was significantly elevated, and the NLR family pyrin domain containing 3 (NLRP3) expression was dramatically decreased following Tan IIA treatment. Most importantly, the suppression of SIRT1 remarkably abrogated both the protective effects of Tan IIA against DN and its inhibition on pyroptosis-related molecules. Collectively, our results suggest that Tan IIA protects against DN by inhibiting caspase-1 and GSDMD-mediated pyroptosis through the SIRT1/NLRP3 pathway.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"285-301"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological Effects of Licorice (<i>Glycyrrhiza</i> spp.) and Its Bioactive Constituents: The Perspective of Intestinal Microbiota.","authors":"Xiaoyu Ji, Cai Zhang","doi":"10.1142/S0192415X26500187","DOIUrl":"10.1142/S0192415X26500187","url":null,"abstract":"<p><p>Licorice (<i>Glycyrrhiza</i> spp.) is a traditional medicinal plant whose roots and rhizomes possess multiple pharmacological effects. Its core active components include flavonoids, triterpenoids such as glycyrrhizin, and polysaccharides. This paper focuses on licorice's gut microbiota-mediated mechanisms of action. Licorice enhances intestinal barrier integrity and protects gastrointestinal mucosa by upregulating tight junction proteins, activating repair pathways like epidermal growth factor receptor/extracellular regulated protein kinases (EGFR/ERK), and modulating inflammatory signaling via the tumor necrosis factor/nuclear factor-κB (TNF/NF-κB) pathway. At the systemic level, licorice modulates core pathways like Toll-like receptor 4 (TLR4)/NF-κB and farnesoid X receptor/Takeda G protein-coupled receptor 5 (FXR/TGR5) through cross-organ axes such as the gut-immune, gut-liver, and gut-adipose axes to improve conditions including inflammatory bowel disease (IBD), obesity, type 2 diabetes mellitus (T2DM), and non-alcoholic fatty liver disease (NAFLD). However, licorice poses dose-dependent risks which raise concerns regarding its safety. Long-term high-dose use may induce pseudohyperaldosteronism and interactions with multiple medications, and thus necessitates strict clinical dose control. This study reveals the gut microbiota's central mediating role in licorice's efficacy, and thereby provides theoretical support for its rational clinical application.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"509-528"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147313702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Mechanisms and Therapeutic Potentials of Triptolide in Autoimmune Diseases: Advances and Challenges.","authors":"Junning Zhang, Fangying Huang, Yujiao Xu, Jinfang Xie, Yinping Lei, Zipeng Hu, Yong Dai, Xianliang Hou","doi":"10.1142/S0192415X26500072","DOIUrl":"10.1142/S0192415X26500072","url":null,"abstract":"<p><p>The global incidence and prevalence of autoimmune diseases are increasing, and there is thus a need to develop novel, effective, and affordable therapeutic agents for autoimmune diseases. Triptolide (TP), a bioactive diterpenoid epoxide isolated from <i>Tripterygium wilfordii</i> Hook F, exhibits potent immunosuppressive and anti-inflammatory activities, and can be a potential therapeutic for multiple autoimmune diseases. The therapeutic effects of TP can be attributed to multiple mechanisms, including the inhibition of T cell and B cell activation, the restoration of T helper 17 cell/regulatory T cell balance, the suppression of pro-inflammatory cytokines, and the modulation of critical signaling pathways like the NF-κB, JAK/STAT, and PI3K/Akt pathways. TP alleviates pathological conditions by regulating oxidative stress responses and influencing gut microbiota composition. However, the clinical application of TP is limited due to severe dose-dependent and time-dependent toxic effects on the liver, kidneys, reproductive system, and other organs. Recent studies have highlighted several strategies, such as chemical structure modification, nanocarrier-based delivery systems, engineered exosomes, and combination pharmacotherapy, to both improve therapeutic efficacy and mitigate systemic toxicity. To provide insights for its safe clinical translation, this review systematically summarizes the pharmacological mechanisms, therapeutic potential, and toxicological challenges of TP in autoimmune diseases.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"54 1","pages":"201-228"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146183963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phytochemical Insights into <i>Panax</i> Genus Metabolites: Evidence-Based Fatigue Intervention via Ethnopharmacological and Biomedical Perspectives.","authors":"Huong-Giang Le, Thi Luu Kim Huong Huynh, Thanh Hao Huynh, Ngoc-Thac Pham, Bo-Rong Peng, Mohamed El-Shazly, Lo-Yun Chen, Lung-Shuo Wang, Pei-Tzu Yen, Kuei-Hung Lai","doi":"10.1142/S0192415X26500060","DOIUrl":"10.1142/S0192415X26500060","url":null,"abstract":"<p><p>Traditional Chinese Medicine (TCM) has a longstanding history in the treatment of fatigue-related conditions, and is increasingly recognized as a foundation for novel therapeutic approaches. The <i>Panax</i> genus, extensively utilized in the fundamental TCM principles to enhance vitality, modulate immune function, and stimulate Yang energy, is a key resource in managing both physiological and pathological fatigue. This study provides a comprehensive synthesis of recent advancements in plant-derived metabolites from various <i>Panax</i> species with an emphasis on their structural diversity and structure-activity relationships. Notably, this represents the first systematic exploration of <i>Panax</i> metabolites with potential antifatigue effects. A systematic literature review was conducted using major scientific databases such as PubMed, Google Scholar, and ScienceDirect. The search query \"(scientific name of herbal medicine in the <i>Panax</i> genus) AND (\"antifatigue\")\" was employed. Additionally, classical herbals, botanical literature, and pharmacopoeias were reviewed to contextualize the findings. Comprehensive analysis of 105 studies elucidated 16 predominant metabolites exhibiting antifatigue activity. These metabolites primarily originated from <i>Panax ginseng</i>, <i>Panax quinquefolium</i>, and <i>Panax notoginseng</i>. Ginsenosides Rb1 and Rg1 demonstrated the most substantial pharmacological efficacy in experimental models, in particular by ameliorating metabolic perturbations and mitigating oxidative stress <i>in vivo</i>. Clinical trials predominantly relied on subjective patient-reported measures, such as the Multidimensional Fatigue Inventory (MFI) and Visual Analogue Scale (VAS), and yielded largely positive outcomes. These findings substantiate fundamental TCM principles and reinforce the therapeutic potential of <i>Panax</i> species in fatigue management. The integration of traditional knowledge with contemporary biomedical research enhances the understanding and clinical applicability of <i>Panax</i> species in addressing fatigue-related disorders.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"171-200"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin Metabolites and Metabolic Health: Insights into Regulatory Mechanisms of Glucose and Lipid Homeostasis.","authors":"Fanfei Liu, Chongyan Zhao, Qi Zhang, Hui Ju, Xuling Peng, Gen Li","doi":"10.1142/S0192415X26500424","DOIUrl":"10.1142/S0192415X26500424","url":null,"abstract":"<p><p>Curcumin, a bioactive compound and vibrant yellow pigment extracted from the rhizome of <i>Curcuma longa</i>, has a well-established safety profile and demonstrates defined pharmacological activities. These activities include regulating glucose and lipid metabolism, exerting anti-oxidant effects, and modulating autophagy. However, its pharmacokinetic limitations-notably low oral bioavailability and insufficient blood concentration-present a dichotomy with its significant biological effects. Research indicates that curcumin undergoes rapid and extensive metabolic transformation <i>in vivo</i>, which suggests that its pharmacological actions may be partially mediated by metabolites. Notably, curcumin metabolites exhibit activity comparable to, or even exceeding, the therapeutic potential of the parent compound in models of glucose and lipid metabolism disorders. Through a systematic review of curcumin's metabolic pathways and the targets of its metabolites, we identified several key conclusions. First, the beneficial effects of curcumin on glucose and lipid metabolism are closely linked to its reduced metabolites dihydrocurcumin, tetrahydrocurcumin, and hexahydrocurcumin. Second, the parent compound curcumin and its metabolites exhibit overlapping actions on core signaling pathways, such as PPARα, NF-κB, and PI3K-AKT, which confirms metabolites as significant contributors to the overall efficacy. Third, preclinical research focusing on these reduced metabolites offers promising new directions for combination therapies targeting glucose and lipid metabolism disorders and their complications. Building upon these conclusions, this paper further synthesizes the structure-activity relationships of the principal reduced metabolite-tetrahydrocurcumin, which is characterized by its high abundance among metabolites and concentrated research focus on its modification, and aims to provide a theoretical foundation for structure optimization and drug development based on metabolites.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1141-1165"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148229886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Restoring Homeostatic Balance: Advances in Traditional Chinese Medicine for Rheumatoid Arthritis.","authors":"Yuhong Xiang, Aihong Yang, Cong Guo, Jintang Cheng, Jun Zhang, Chang Chen, Sha Chen, Jinzhu Jiang, Jipeng Di, Xianju Liu, Siyuan Li, An Liu, Yan Liu, Qingxia Xu","doi":"10.1142/S0192415X26500278","DOIUrl":"10.1142/S0192415X26500278","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic autoimmune disease with inflammation-mediated joint damage. Its pathogenesis involves synergistic impairment of multiple physiological balances, including immune cell subset dysregulation, abnormal inflammation, oxidative stress, pathological angiogenesis, bone homeostasis disorder and gut microbiota dysbiosis. Conventional therapies have high costs and adverse effects. Traditional Chinese medicine (TCM) follows a holistic balance-restoring concept and is a promising alternative, with <i>Tripterygium wilfordii</i>, Wutou Decoction and <i>Toddalia asiatica</i> extract as evidence-based representatives. This review summarizes 2020-2025 <i>in vitro</i> and <i>in vivo</i> studies on anti-RA TCM. Its core therapeutic mechanism is multi-target, network-based regulation. It rectifies various pathological imbalances simultaneously: modulating immune cell polarization, rebalancing inflammatory factors, scavenging ROS, inhibiting abnormal angiogenesis, regulating osteoblast-osteoclast crosstalk and reshaping gut microbiota. Single TCM agents act on multiple balance networks, showing complex pharmacological properties. TCM's unique advantage for RA is reestablishing the body's dynamic homeostasis by targeting interconnected pathological balances. Further research is needed to clarify TCM components' synergistic regulatory mechanisms and promote their clinical translation.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"733-762"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}