The American journal of Chinese medicine最新文献

{"title":"Cell Death in Atherosclerosis: Mechanistic Insights and Therapeutic Potential of Traditional Chinese Medicine.","authors":"Danqi Xie, Zhaoshui Li, Xiaolei Zheng, Xiaohui Sun, Xin Leng, Ting Jiang","doi":"10.1142/S0192415X2650014X","DOIUrl":"10.1142/S0192415X2650014X","url":null,"abstract":"<p><p>Atherosclerosis (AS), a major cause of cardiovascular diseases, is driven by dysregulated programmed cell death (PCD) pathways. These pathways, including apoptosis, pyroptosis, ferroptosis, autophagy, and necroptosis, contribute to plaque instability. Traditional Chinese Medicine (TCM) offers a multi-targeted approach for modulating these pathways, but its molecular mechanisms in AS remain inadequately explored. This review aims to investigate the modulatory effects of TCM on PCD pathways in AS, its therapeutic potential for enhancing plaque stability, and the underlying molecular mechanisms. A narrative literature review based on relevant preclinical <i>in vitro</i> and <i>in vivo</i> studies was conducted on TCM bioactive constituents and formulas. These included studies on tonifying herbs like <i>Radix Astragali</i>, <i>Radix Ginseng</i>, and <i>Radix Glycyrrhizae</i>, the extracts of <i>Radix Salviae liguliobae,</i> and classical prescriptions such as Danshen Prescription, Huayu Qutan Recipe, Modified Taohong Siwu Decoction, Xuezhikang, Gualou Xiebai Decoction, and Mai Ji Tong Granules. The relevant data were obtained from searches of major international and Chinese biomedical databases including PubMed, Web of Science, Embase, Cochrane Library, the China Biology Medicine Database, CNKI, Wanfang, and CSTJ. The evidence indicates that these interventions modulate PCD-related pathways to thereby inhibit pathological cell death, enhance protective autophagy, and influence cellular homeostasis, inflammation, oxidative stress, lipid accumulation, and efferocytosis. TCM's multi-component nature addresses the limitations of single-target Western therapies, and thus provides a holistic strategy for AS management. However, gaps remain in the mechanistic understanding and pharmacokinetic profiles of TCM constituents that hinder clinical application. This review emphasizes TCM's potential as a complementary therapy for AS. It likewise suggests the need for further studies to identify bioactive compounds and integrate TCM with precision medicine in order to achieve better therapeutic outcomes.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"375-409"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146260525","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":"Acupuncture for Neuropathic Pain: Mechanisms, Clinical Efficacy and Future Perspectives.","authors":"Yu-Hsuan Chen, Sheng-Teng Huang, Jaung-Geng Lin","doi":"10.1142/S0192415X26500254","DOIUrl":"10.1142/S0192415X26500254","url":null,"abstract":"<p><p>Neuropathic pain is a prevalent, intolerable disease that poses significant clinical challenges due to the limited efficacy and adverse effects of conventional pharmacotherapy. Acupuncture is widely recognized for its efficacy in neuropathic pain management. This review aims to provide a comprehensive overview of the current understanding, clinical evidence, challenges, and future potential of acupuncture, and to thus highlight its role within an integrated, multidisciplinary approach to managing neuropathic pain. Despite its popularity, the mechanisms by which acupuncture exerts these effects are not fully understood. Its possible mechanisms of action are complicated, involving the modulation of endogenous opioids and neurotransmitters, activation of descending pain-inhibitory pathways, suppression of neuroinflammation, and induction of beneficial neuroplasticity. Clinical evidence from systematic reviews supports its efficacy, in particular for diabetic peripheral neuropathy, chemotherapy-induced peripheral neuropathy, and central post-stroke pain, and shows significant promise for various neuropathic pain disorders. However, the quality of primary studies is variable. Within a multidisciplinary basis, acupuncture offers a promising, safe, and mechanistically supported adjunct for managing complex neuropathic pain.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"685-705"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793562","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":"Mitochondria-Associated Ferroptosis and Diabetic Osteoporosis: Exploration of Traditional Chinese Medicine Treatment and Mechanisms of Action.","authors":"Guoyu Pang, Rui Bai, Mi Chen, Wenhui Chen","doi":"10.1142/S0192415X26500539","DOIUrl":"10.1142/S0192415X26500539","url":null,"abstract":"<p><p>Diabetic osteoporosis (DOP) is a serious skeletal complication of diabetes mellitus. Its pathogenesis is complex, and its clinical prevention and treatment face significant challenges. In recent years, ferroptosis - particularly mitochondria-associated ferroptosis, which is closely linked to mitochondrial dysfunction - has been identified as a key mechanism underlying osteoblast injury in DOP. A chronic high-glucose environment can induce mitochondrial oxidative stress, iron metabolic dysregulation, and a lipid peroxidation cascade, leading to failure of the antioxidant systems (e.g., the GPX4 and Nrf2 pathways) and ultimately resulting in ferroptosis of osteoblasts and disruption of bone homeostasis. Traditional Chinese medicine (TCM) offers the advantages of multi-target and holistic regulation in the prevention of DOP. Its therapeutic principle of \"tonifying the kidney and replenishing essence, activating blood circulation and removing blood stasis\" is highly consistent with modern strategies aimed at intervening in mitochondrial ferroptosis. This review examines the central role of mitochondrial ferroptosis in DOP and elucidates the pathogenesis of DOP from a modern biological perspective. Furthermore, it summarizes experimental evidence demonstrating that astragaloside IV, ginsenoside Rg1, puerarin, icariin, curcumin, and Zuogui Pills can effectively inhibit mitochondrial ferroptosis by activating the Nrf2/GPX4 antioxidant axis, improving mitochondrial function, and regulating iron homeostasis, thereby conferring bone-protective effects. In conclusion, targeting mitochondria-associated ferroptosis represents a promising therapeutic strategy for DOP, and TCM interventions that modulate this pathway offer a novel direction for drug development and clinical management.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1455-1474"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148407584","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":"Targeting Ferroptosis in Cardiovascular Diseases: The Emerging Role of Traditional Chinese Medicine.","authors":"Yanbin Chang, Yan Li, Ying Huang, Lili Zhang, Ruiying Zhang","doi":"10.1142/S0192415X26500527","DOIUrl":"10.1142/S0192415X26500527","url":null,"abstract":"<p><p>Ferroptosis is a distinct form of regulated cell death (RCD) characterized primarily by iron dysregulation and lipid peroxidation. Emerging evidence indicates ferroptosis critically contributes to the initiation and progression of multiple cardiovascular diseases (CVDs), including atherosclerosis (AS), myocardial ischemia/reperfusion (MI/R) injury, myocardial infarction (MI), cardiomyopathy, and heart failure (HF). With growing recognition of ferroptosis's role in CVD pathogenesis, targeting ferroptosis has become a promising therapeutic strategy for these diseases. Traditional Chinese medicine (TCM) is characterized by multicomponent, multitarget, and holistic regulatory properties. Studies have demonstrated that bioactive constituents, such as 6-gingerol, curcumin, ginsenoside Rg3, paeoniflorin, and stachydrine, and TCM compound formulations, including Danshentongluo-Detoxification Decoction, Yiqi Fumai Injection, Shexiang Baoxin Pill, and Shensong Yangxin Capsule, exert cardioprotective effects. These effects operate by suppressing ferroptosis via the modulation of iron metabolism, inhibition of lipid peroxidation, and enhancement of anti-oxidant defense systems. Accordingly, this review systematically summarizes the molecular mechanisms of ferroptosis and its pathological roles in various CVDs while placing a particular emphasis on recent advances in TCM-based ferroptosis interventions. This summary provides theoretical insights and potential research strategies both for the prevention and treatment of CVD, and for the development of related therapeutics.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1427-1454"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148407621","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":"Context-Dependent Signaling Network of Ginsenoside Rg2: A Molecular Basis for Its Bidirectional Pharmacological Effects.","authors":"Yu-Xi Gong, Yu-Zhuo Zhang, Jing-Tian Zhang, Ya-Jun Wang, Li-Chun Zhao, Wei Li","doi":"10.1142/S0192415X26500631","DOIUrl":"10.1142/S0192415X26500631","url":null,"abstract":"<p><p>Ginsenoside Rg2 (G-Rg2) is a key protopanaxatriol-type saponin from Panax ginseng. Increasing evidence has shown that G-Rg2 exerts pharmacological effects such as neuroprotection, immune regulation, anti-inflammation and inhibition of tumor proliferation by reducing inflammatory response, blocking apoptotic cascade and regulating autophagic flow. In terms of mechanism of action, the diverse biological effects of G-Rg2 result from its background-dependent regulation of key intracellular signaling pathways such as AMPK, MAPK, NF-κB and PI3K-AKT-mTOR, which are interconnected to form a complex regulatory network. This plasticity in pathway regulation confers bidirectional pharmacological properties of G-Rg2, which induces apoptosis through inhibition of the PI3K-AKT-mTOR pathway in MCF-7 breast cancer cells, whereas it activates the same pathway to promote cell survival in cardiomyocytes and neurons under ischemic conditions. Metabolomics and multiomics studies in animal models suggest that G-Rg2 regulates metabolic networks and multiple signaling pathways simultaneously in a complex disease environment, suggesting that G-Rg2 is most likely a network-level regulatory mode rather than a linear single-target action. The poor oral bioavailability, rapid systemic clearance, stereochemical complexity due to the 20(R)/20(S) isomers, and insufficient long-term safety data of G-Rg2 have hindered its translation into clinical trials. Based on existing mechanism-related research on G-Rg2, this review proposes a network-based regulatory framework and offers specific suggestions to enhance the bioavailability and targeting of G-Rg2, providing actionable directions for its clinical translation.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1695-1720"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148715178","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 Ameliorates Sleep Deprivation-Induced Cognitive Impairment: Involvement of Gut Microbiota and the TLR4/NF-κB Signaling Pathway.","authors":"Chao Yin, Meiya Zhang, Shunbo Zhang, Tian Ren, Li Ding, Ping Wang, Qiuyun You","doi":"10.1142/S0192415X26500801","DOIUrl":"10.1142/S0192415X26500801","url":null,"abstract":"<p><p>Previous studies have indicated that <i>Salvia miltiorrhiza</i> Bunge (Danshen, DS) improves sleep deprivation (SD)-induced cognitive deficits, suggesting that tanshinone IIA (Tan IIA) may be a key pharmacodynamic substance. However, the mechanism behind this remains unclear. This study aims to evaluate the protective effects of Tan IIA on learning and memory abilities in SD model rats and to explore its potential mechanisms related to gut microbiota. The Morris water maze (MWM) test was used to assess cognitive function, while Hematoxylin and Eosin (H&E) staining, Nissl staining, immunofluorescence, and Alcian blue-periodic acid Schiff (AB-PAS) staining were employed to examine histopathology and barrier proteins. Enzyme-linked immunosorbent assay (ELISA), Western blot, and 16S rRNA microbiome sequencing were used to explore the mechanism of Tan IIA in the SD rat model. Tan IIA significantly protected cognitive function in SD model rats, rescued the BBB function (ZO-1 and Occludin), reduced hippocampal inflammation and neuronal death, and alleviated hippocampal microglial inflammatory activation and Aβ42 deposition. Additionally, Tan IIA treatment markedly reduced systemic inflammation (serum TNF-α, IL-1β, and IL-6), intestinal inflammation, and intestinal barrier disruption (MUC-2, ZO-1, and Occludin). 16S rRNA microbiome sequencing indicated that the therapeutic effects of Tan IIA were associated with gut microbiota regulation, reducing lipopolysaccharide (LPS) production and leakage, thereby modulating abnormal expression of the TLR4/NF-κB signaling pathways and the abnormal expression of downstream inflammatory cytokines (TNF-α, IL-1β, IL-6) and enzymes (iNOS and COX2). In conclusion, Tan IIA protects cognitive function in SD rats through anti-inflammatory mechanisms, in part by reshaping the gut microbiota and modulating the TLR4/NF-κB signaling pathway, providing a theoretical basis for the clinical application of Tan IIA in the prevention and treatment of SD-related cognitive impairment.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"2199-2228"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121272","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":"Decoding Ginsenosides: The Structural and Therapeutic Core of Ginseng.","authors":"Ka Iong Chan, Xintong Han, Siyuan Chen, Dianxin Cui, Sio I Chan, Wenying Zheng, Simin Chen, Lihua Shen, Wanyu Li, Yu Fan, Guodong Li, Milen I Georgiev, Wen Tan, Zhangfeng Zhong","doi":"10.1142/S0192415X26500746","DOIUrl":"10.1142/S0192415X26500746","url":null,"abstract":"<p><p>Ginseng (<i>Panax ginseng</i> C.A. Meyer), a highly valued traditional herb in traditional medicine, exerts its major health benefits through ginsenosides - its core bioactive triterpenoid saponins. With a characteristic steroidal structure, ginsenosides interact with cell membranes, receptors, and signaling cascades to produce diverse pharmacological effects. This review summarizes the pharmacological properties, molecular mechanisms, structure-activity relationships, and advanced delivery strategies of key ginsenosides, including Rb1, Rg1, Rg3, Rh2, compound K (CK), and Rd. These compounds exhibit potent anti-oxidant, anti-inflammatory, cardioprotective, neuroprotective, antidiabetic, anti-obesity, anticancer, and anti-aging activities, acting through well-characterized pathways such as PI3K/Akt, Nrf2/ARE, AMPK, MAPK, and NF-κB. Notably, their bioactivity is strongly governed by the number and position of sugar moieties: ginsenosides with fewer glycosyl groups (e.g., Rg3, Rh2, and CK) generally display higher potency <i>in vitro</i> and <i>in vivo</i>, whereas multi-glycosylated forms like Rb1 and Rc show milder effects. Despite their promising efficacy, poor oral bioavailability, rapid metabolism, and nonspecific tissue distribution remain major hurdles for clinical translation. To overcome these limitations, recent nanotechnology-based delivery systems have been developed, including liposomes, polymeric nanoparticles, inorganic nanocarriers, self-assembled micelles, and exosome-based platforms, to enhance solubility, prolong circulation, enable targeted delivery, and improve therapeutic outcomes. By integrating current knowledge on ginsenoside pharmacology and formulation engineering, this work supports their translational research and clinical application as multi-target agents for treating inflammatory, metabolic, cardiovascular, neurodegenerative, and malignant disorders.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1981-2028"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149129660","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":"Celastrol Induces Ferroptosis by Regulating CERKL to Exert Anti-Gastric Cancer Effect.","authors":"Chang Yang, Rui Xue, Chuling Qin, Lingyue Huang, Rongrong Nie, Yuqin Luo, Siyuan Xu, Ke Tang, Jianning Chen, Lulu Jia, Qinyou Tan","doi":"10.1142/S0192415X25500351","DOIUrl":"https://doi.org/10.1142/S0192415X25500351","url":null,"abstract":"<p><p>Gastric cancer is a significant global health issue. Celastrol, a natural compound, has shown antitumor potential, but its molecular mechanism in gastric cancer remains unclear. In this study, we treated HGC-27 cells with celastrol and employed CCK8, colony formation, and Transwell assays, revealing its inhibitory effect on cell proliferation and migration. Flow cytometry assay results showed that celastrol could elevate the level of reactive oxygen species (ROS) in HGC-27 cells. By using the iron ion and malondialdehyde (MDA) detection kits, it was found that celastrol promoted the accumulation of iron ions (Fe[Formula: see text] in HGC-27 cells, increased the MDA content, and simultaneously decreased the glutathione (GSH) content. Additionally, Western blot analysis indicated that celastrol exerts an inhibitory effect on the expression of ferroptosis-marker proteins GPX4 and SLC7A11. PCR array and further experiments identified CERKL as a key factor, whose downregulation by celastrol was associated with enhanced ferroptosis. <i>In vivo</i>, celastrol inhibited tumor growth without affecting body weight or organ histology. Our findings suggest that celastrol may inhibit gastric cancer via CERKL-regulated ferroptosis, providing a potential therapeutic strategy.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 3","pages":"931-949"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082978","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":"Mechanisms of Dihydromyricetin for Improving Hepatic Fibrosis through the Integration of Metabolomics and Gut Microbiota.","authors":"Ying Gao, Hao Wu, Yanqun Luo, Xiaoliang Deng, Junming Chen, Tao Wu","doi":"10.1142/S0192415X25500338","DOIUrl":"https://doi.org/10.1142/S0192415X25500338","url":null,"abstract":"<p><p>It is crucial to prevent and treat liver fibrosis in patients with chronic liver disease. Dihydromyricetin (DMY) is a natural flavonoid compound from traditional Chinese medicine, known to alleviate chronic liver injury. However, its role in regulating inflammatory responses through gut microbiota and metabolic changes remains unclear. In this study, a mouse model of liver fibrosis was induced with carbon tetrachloride (CCl₄), and DMY was administered via gavage. Histopathology, immunohistochemistry, Reverse Transcription Polymerase Chain Reaction (RT-PCR), 16S rRNA sequencing, and untargeted metabolomics were employed to evaluate DMY's pharmacological effects on CCl₄-induced liver fibrosis and explore its underlying mechanisms. Our results show that DMY reduced the aspartate transaminase (AST) and alanine transaminase (ALT) serum levels in liver fibrosis model mice, and lowered the mRNA expression of pro-inflammatory cytokines and fibrosis markers. Additionally, DMY restored the richness and diversity of the gut microbiota, with several microbiota taxa significantly correlating with inflammatory markers. Metabolomic analysis of serum and liver tissue revealed that DMY significantly altered the liver metabolite disturbances induced by CCl₄. Pearson correlation analysis demonstrated a strong relationship between microbial composition and liver metabolites. These results suggest that DMY alleviates liver fibrosis in mice by reshaping the gut microbiota and host metabolism, thereby improving the inflammatory response.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 3","pages":"889-908"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082981","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":"Regulatory Role of Flavonoid Baicalin from <i>Scutellaria baicalensis</i> on AMPK: A Review.","authors":"Ming Jiang, Zhuoneng Li, Xu Qin, Lili Chen, Guangxun Zhu","doi":"10.1142/S0192415X25500296","DOIUrl":"https://doi.org/10.1142/S0192415X25500296","url":null,"abstract":"<p><p>AMP-activated protein kinase (AMPK) is a ubiquitous sensor of cellular energy and nutrient status in eukaryotic cells. It serves an essential function in the modulation of energy balance and metabolism homeostasis through its regulation of carbohydrate metabolism, lipid metabolism and protein metabolism. The dysregulation of AMPK is closely related to a series of systemic diseases, affecting multiple organs and tissues. Baicalin is a natural compound derived from the dry raw root of <i>Scutellaria baicalensis</i>, and it has been found to exhibit several potential pharmacological actions. These include hepatoprotective effects, anti-inflammation effects and anti-tumor effects. These biological activities are related to the regulatory effect of baicalin on the host metabolism, which is closely associated with AMPK modulation. In this review, we provide an overview of the regulatory effect of baicalin on AMPK and its upstream and downstream signaling pathways. The pharmacological properties and underlying mechanism of baicalin for regulating AMPK were summarized with regards to four aspects: regulatory effect of baicalin on AMPK in lipid metabolism and glucose metabolism, regulatory effect of baicalin on AMPK in its pharmacological effect of anti-tumor and anti-inflammation. As a natural compound, baicalin has the potential for the management of certain AMPK-related diseases.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 3","pages":"771-801"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082986","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}