The American journal of Chinese medicine最新文献

{"title":"Astragaloside IV Attenuates Heart Failure by Modulating SCAD/DJ-1/SIRT1/FOXO3a Signaling Axis.","authors":"Yu-Hong Cao, Ya-Xin Duan, Jie-Ye Qin, Guan-Qi Peng, Qing-Ping Xu, Lan-Ting Liu, Chun-Yu Chen, Huan Peng, Zhi-Cheng Yang, Xue-Diao Pan, Fei-Hai Shen, Si-Gui Zhou","doi":"10.1142/S0192415X26500461","DOIUrl":"10.1142/S0192415X26500461","url":null,"abstract":"<p><p>As the key functioning element of the traditional Chinese medicinal herb Astragalus, Astragaloside IV (AS-IV) has potentially protective effects on heart failure (HF). Short-chain Acyl-CoA dehydrogenase (SCAD) is a critical enzyme in fatty acid β-oxidation, which negatively regulates cardiomyocyte apoptosis and HF. However, the molecular mechanism by which AS-IV influences myocardial energy metabolism in HF remains uncertain. In this study, we aim to both explore the underlying mechanisms of AS-IV in protecting against HF and provide potential directions for the clinical use of AS-IV. <i>In vivo</i>, an HF model was induced in mice using transverse aortic constriction (TAC) surgery in order to examine echocardiography, cell apoptosis, energy metabolism, oxidative stress, and signaling molecules. <i>In vitro</i>, a cell apoptosis model was stimulated by tert-butyl hydroperoxide (tBHP) in H9C2 cardiomyocytes. SCAD or DJ-1 was silenced using small interfering RNA. <i>In vivo</i> results demonstrated that AS-IV significantly ameliorated cardiac function and myocardial fibrosis, enhanced energy metabolism, and reduced both cell apoptosis and oxidative stress. Mechanistically, AS-IV activated SCAD/DJ-1/SIRT1/FOXO3a signaling axis in HF mice. This mechanism was further validated <i>in vitro</i>, as the knockdown of SCAD or DJ-1 attenuated the anti-apoptotic effect of AS-IV and the regulation of signaling axis in an H9C2 cardiomyocyte apoptosis model. These findings show that AS-IV improves myocardial energy metabolism to decrease oxidative stress and cardiomyocyte apoptosis via the SCAD/DJ-1/SIRT1/FOXO3a signaling axis, and therefore suggest its potential as a therapeutic agent for HF.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1253-1279"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148202009","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":"Progress of Traditional Chinese Medicine in Targeting Ferroptosis to Combat Cerebral Ischemia-Reperfusion Injury.","authors":"Jianhui Li, Annan Liu, Wei Gao, Qiuyan Ye, Liping Xing, Peihan Duan, Wang Guo, Honglin Li","doi":"10.1142/S0192415X26500382","DOIUrl":"10.1142/S0192415X26500382","url":null,"abstract":"<p><p>Cerebral ischemia-reperfusion injury (CIRI) often results in significant morbidity and mortality. The effectiveness of current reperfusion therapies is hindered by substantial secondary damage, which highlights the need for novel molecular targets and neuroprotective strategies. Ferroptosis, a form of programmed cell death driven by iron dysregulation and lipid peroxidation, has emerged as a key player in CIRI pathogenesis. Traditional Chinese medicine (TCM) has demonstrated considerable potential in managing IS, and increasing evidence suggests its neuroprotective effects are primarily mediated through modulation of ferroptotic pathways. This review evaluates the efficacy of various TCM approaches in combating CIRI, and offers a specific focus on the roles of active compounds (e.g., astragaloside IV, rhein, baicalein, ginkgolide B, and berberine), classic herbal formulas (e.g., Buyang Huanwu Decoction, Tongqiao Huoxue Decoction, and Naotaifang), and acupuncture therapies. This review outlines how these interventions attenuate CIRI by targeting critical ferroptosis-related mechanisms. These mechanisms include enhancing anti-oxidant defenses (Nrf2/SLC7A11/GPX4), modulating lipid metabolism (ACSL4), restoring iron homeostasis, and maintaining the ischemic microenvironment (including blood-brain barrier integrity and microglial polarization). However, current research faces challenges such as the insufficient understanding of the pharmacological basis of complex formulas, unclear dose-response relationships, and a lack of comprehensive validation along the \"ingredient-target-phenotype\" continuum. Future research should focus on leveraging advanced technologies - such as network pharmacology, multi-omics, and artificial intelligence - to unravel the antiferroptotic networks of TCM. Such integrative approaches will drive the modernization of TCM and facilitate the development of precision medicine to thus present new opportunities for neuroprotection in CIRI.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1037-1059"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148207262","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":"Ginsenosides in Liver Fibrosis: Pharmacological Actions and Therapeutic Potential.","authors":"Na Li, Fanghang Ye, Fei Yu, Liyuan Hao, Shenghao Li, Qing Peng, Jiali Deng, Junli Zhang, Xiaoyu Hu","doi":"10.1142/S0192415X26500436","DOIUrl":"10.1142/S0192415X26500436","url":null,"abstract":"<p><p>Liver fibrosis (LF) represents a critical pathological stage in the progression of various chronic liver diseases, and is characterized by the sustained activation of hepatic stellate cells (HSCs) and excessive deposition of extracellular matrix (ECM). These processes ultimately lead to cirrhosis and even hepatocellular carcinoma. Current therapeutic strategies for LF primarily rely on etiological interventions and supportive management. However, due to the complex pathogenesis of LF, involving multiple interconnected signaling pathways, effective and specific antifibrotic therapies remain lacking. Therefore, the development of multi-target and system-level therapeutic strategies for the treatment of LF is of considerable importance. Ginsenosides, the major bioactive components of <i>Panax ginseng</i>, exhibit multi-component and multi-target pharmacological properties and have shown broad potential in the prevention and treatment of liver fibrosis. Accumulating evidence indicates that several ginsenosides, including Rg1, Rb1, Rg3, Rh1, Rd, and the metabolite Compound K, exert significant antifibrotic effects across various experimental models. This review systematically summarizes the pharmacological mechanisms of ginsenosides in liver fibrosis and integrates their effects from a mechanistic perspective. Overall, ginsenosides directly target key fibrogenic processes by inhibiting HSCs activation and proliferation, promoting apoptosis, reducing ECM synthesis, and facilitating ECM degradation. In addition, they indirectly modulate fibrosis progression by regulating upstream amplifying factors such as inflammation, oxidative stress, and the immune microenvironment. Furthermore, ginsenosides also influence cell fate-related processes, including autophagy and ferroptosis, in a cell-type-dependent manner. In hepatocytes, maintaining appropriate autophagic activity and suppressing lipid peroxidation generally confers protective effects. In HSCs, by contrast, the inhibition of protective autophagy or induction of ferroptosis appears to be more relevant to antifibrotic efficacy. Although substantial experimental evidence supports the antifibrotic potential of ginsenosides, their clinical translation remains limited by low bioavailability, unclear active forms <i>in vivo</i>, and the lack of high-quality clinical studies. Future investigations should focus on identifying key molecular targets and underlying mechanisms through multi-omics approaches and structure-activity relationship analyses. Well-designed clinical trials should likewise be conducted to evaluate the safety and therapeutic efficacy of ginsenosides and, thereby, facilitate their clinical application in liver fibrosis.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1167-1191"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148261286","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":"Rhein Alleviates Cerebral Ischemia/Reperfusion Injury by Inhibiting the Microglial NLRP3 Inflammasome/Pyroptosis Axis and Regulating Microglial M1/M2 Phenotypes.","authors":"Xun Li, Yan Li, Wei-Peng Jing, Ming-He Yao, Ling-Ling Li, Hai-Bo Zhang, Yan-Jie Liu, Hua-Ming Xu, Dong-Fang Ren, Hui-Fen Ma, Pei-Pei Yuan, Ya-Min Li, Jun-Min Fu, Hui Wang, Xiao-Yan Fang, Ming-San Miao","doi":"10.1142/S0192415X26500096","DOIUrl":"10.1142/S0192415X26500096","url":null,"abstract":"<p><p>The activation of the NLRP3 inflammasome is critical to inducing microglial activation and pyroptosis following cerebral ischemia/reperfusion (I/R). Suppressing the neurotoxicity of activated microglia has become an effective approach for treating cerebral I/R injury. Rhein is an anthraquinone compound found in rheum, and possesses anti-inflammatory, antagonistic, and antifibrotic effects. This study assessed whether rhein influences NLRP3 inflammasome activation, pyroptosis, and the polarization of microglia after cerebral I/R or oxygen-glucose deprivation and reoxygenation (OGD/R). Cerebral I/R models were established in Sprague-Dawley rats via transient middle cerebral artery occlusion (tMCAO) surgery, and OGD/R models were established in BV-2 cells using a hypoxic chamber. After treatment with rhein, the infarction/edema ratio, BV-2 cell viability, expression of NLRP3 inflammasome, and levels of microglial polarization and pyroptosis were detected. Finally, NLRP3 inhibitors (MCC950) were used to assess whether rhein exerted its effects by inhibiting the activation of the NLRP3 inflammasome in regulating pyroptosis and polarization of microglia. Rhein permeated the blood-brain barrier of rats after tMCAO, protected against tMCAO-induced brain injury, and inhibited microglial NLRP3 inflammasome activation and pyroptosis after tMCAO or OGD/R. It also suppressed tMCAO- or OGD/R-induced polarization of the M1 phenotype in microglia, and skewed them toward the M2 phenotype. Moreover, co-administration of rhein and MCC950 synergistically enhanced both the inhibition of the NLRP3 inflammasome activation/pyroptosis axis and the regulation of microglial polarization after tMCAO or OGD/R. Rhein exerts neuroprotective effects by regulating microglial pyroptosis and polarization through inhibiting the activation of NLRP3 inflammasome after tMCAO or OGD/R.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"54 1","pages":"263-284"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146183941","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":"Research Progress on the Mechanism of Astragaloside IV for Treating Myocardial Infarction.","authors":"Bin Li, Yijia Liu, Guiping Hu, Ming Ren, Yanguo Wang, Li Sun, Qiang Xu, Weihong Yang, Shuo Wang","doi":"10.1142/S0192415X26500205","DOIUrl":"10.1142/S0192415X26500205","url":null,"abstract":"<p><p>Myocardial infarction (MI) is a severe cardiovascular disorder characterized by an irreversible myocardial necrosis caused by acute ischemia. The typical manifestations of MI include persistent substernal chest pain, dyspnea, nausea, vomiting, and diaphoresis. Astragaloside IV (AS-IV), a major bioactive component of <i>Astragalus membranaceus</i>, has been extensively investigated over the past decade. Evidence indicates that AS-IV exerts multifaceted protective effects against MI by modulating various key signaling pathways involved in anti-inflammatory, anti-oxidative stress, and antifibrotic activities, the inhibition of cardiomyocyte apoptosis, and the maintenance of mitochondrial homeostasis. These pathways include TLR4/NF-κB, PI3K/AKT, TGF-β/Smad2, ROS/caspase-1/GSDMD, Wnt/β-catenin, AMPK/ACSS2/PPARα, Sirt3/Drp1, and PINK1/Parkin. Although mechanistic studies have substantially advanced, the clinical application of AS-IV in MI remains in the exploratory stage. Further well-designed clinical trials are necessary in order to validate the therapeutic efficacy and safety of AS-IV, thereby facilitating its translation from experimental research to clinical practice, and offering new insights and potential strategies for MI management.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"555-572"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146204473","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":"Bufalin Induces Ferroptosis in Triple-Negative Breast Cancer via Inhibition of the NRF2/HO-1/GPX4 Pathway.","authors":"Ji-Ying Zhou, An-Xin Wang, Min Jin, Si-Yu Guo, Fan-Qin Zhang, Muyassar Mamattohti, Pei-Ying Lu, Ke-Yan Chai, Mei-Ling Guo, Hua Luo, Jia-Rui Wu","doi":"10.1142/S0192415X26500722","DOIUrl":"10.1142/S0192415X26500722","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC), a highly aggressive subtype of breast cancer characterized by poor prognosis and limited therapeutic options, remains a major clinical challenge. Bufalin, a principal bioactive component of Venenum Bufonis, exhibits potent anticancer activity against breast cancer. Nevertheless, the precise molecular mechanism by which bufalin triggers ferroptosis in TNBC cells remains poorly elucidated. In the present study, both <i>in vitro</i> and <i>in vivo</i> investigations were performed. Cellular ferroptosis was comprehensively evaluated by detecting intracellular Fe[Formula: see text], ROS, MDA, and reduced GSH levels, together with ultrastructural observation under transmission electron microscopy. Transcriptome sequencing combined with bioinformatic analysis was applied to screen the core regulatory mechanism of bufalin-induced ferroptosis in TNBC, and subsequent molecular biological experiments were conducted for further validation. The results demonstrated that bufalin significantly suppressed the proliferation and migration of TNBC cells. Bufalin treatment markedly increased Fe[Formula: see text], ROS, and MDA levels, depleted intracellular GSH, and induced mitochondrial shrinkage and cristae damage. Transcriptome analysis identified the NRF2/HO-1/GPX4 signaling axis as the central pathway mediating the pharmacological effect of bufalin. Mechanistically, bufalin downregulated the expression of NRF2, HO-1, SLC7A11, and GPX4, whereas it upregulated KEAP1 expression. <i>In vivo</i> studies verified that bufalin effectively inhibited tumor growth with no obvious systemic toxicity. Moreover, bufalin decreased the expression of GPX4 and Ki-67, increased the number of TUNEL-positive cells, and blocked the activation of the NRF2/HO-1/GPX4 pathway in tumor tissues. In conclusion, bufalin induces ferroptosis in TNBC by inhibiting the NRF2/HO-1/GPX4 signaling pathway, thereby exerting antitumor effects. These findings indicate that bufalin serves as a promising therapeutic agent for TNBC treatment.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1931-1954"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148803859","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":"ERRATUM: <i>Paris polyphylla</i> Suppresses Proliferation and Vasculogenic Mimicry of Human Osteosarcoma Cells and Inhibits Tumor Growth <i>In Vivo</i>.","authors":"Nan Yao, Ke Ren, Yimin Wang, Qiaomei Jin, Xiao Lu, Yan Lu, Cuihua Jiang, Dongjian Zhang, Jun Lu, Chen Wang, Jiege Huo, Yong Chen, Jian Zhang","doi":"10.1142/S0192415X26920011","DOIUrl":"10.1142/S0192415X26920011","url":null,"abstract":"","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1009-1011"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147680012","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 Herbal Medicine: Machine Learning-Driven Insights into Structural Identification and Pharmacological Research.","authors":"Yumo Bie, Yang Yang, Pan Wang","doi":"10.1142/S0192415X26500370","DOIUrl":"10.1142/S0192415X26500370","url":null,"abstract":"<p><p>Herbal medicine is indispensable and crucial to many healthcare systems. Its therapeutic value arises from diverse plant-derived compounds with potential pharmacological activities. This review summarizes recent advances in applying artificial intelligence (AI) and machine learning (ML) to elucidate the pharmacological mechanisms of herbal medicines, and offers a particular focus on revealing their bioactive compounds and pharmacological actions. It highlights how AI-driven analytical frameworks are enhancing the precision and efficiency of mechanism elucidation. Information relevant to herbal medicine and related computational studies was collected via keyword searching in common scientific databases including Google Scholar, PubMed, ACS Publications, Wiley Online Library, ScienceDirect, SpringerLink, Scopus, IEEE Xplore, ACM Digital Library, and Web of Science by using keywords \"herbal medicine\", \"machine learning\", \"deep learning\", \"natural compounds\", \"docking\", \"QSAR\", \"toxicity\", \"mass spectrometry\", \"nuclear magnetic resonance\", \"feature extraction\", \"Absorption\", \"Distribution\", \"Metabolism\", and \"Excretion\". The review finds that AI, particularly ML and deep learning approaches, has been applied to identify bioactive compounds, predict potential targets and mechanistic pathways, and thereby enable the identification of hidden patterns in complex chemical-biological datasets. Recent advances in AI have improved the understanding of the complex components and biological effects of herbal preparations. However, the variability of plant materials and the lack of systematic pharmacological studies remain the major challenges. Approaches that combine experimental data with computational analysis show promise for identifying bioactive compounds, predicting their targets, and clarifying the underlying mechanisms.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1013-1035"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148221481","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":"Regulation of Traditional Chinese Medicine Gut Microbiota Short-Chain Fatty Acid Axis in Type 2 Diabetes Management: A Review.","authors":"Ruodi Yang, Ying Zhou, Yuhang Shen, Juntong Liu, Yan Shi, Yufeng Yang","doi":"10.1142/S0192415X26500011","DOIUrl":"10.1142/S0192415X26500011","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM), a globally prevalent chronic metabolic disorder, imposes a significant worldwide public health burden. As a vital \"microbial organ\" within the human body, the balance of the gut microbiota (GM) structure and function is crucial for maintaining host metabolic health. Short-chain fatty acids (SCFAs), the metabolic products of GM, serve as key signaling molecules that play central roles in maintaining intestinal homeostasis, regulating systemic energy metabolism, and improving insulin sensitivity. Dysregulation of the \"GM-SCFA axis\" has emerged as a core pathological mechanism in the onset and progression of T2DM. Traditional Chinese Medicine (TCM) possesses unique advantages in T2DM treatment through its \"holistic regulation and multi-targeted intervention,\" which enables precise modulation of the GM-SCFA axis. This paper provides a systematic review of the pathological mechanisms by which dysregulation of the GM-SCFA axis induces T2DM, and specifically covers energy metabolism disorders, insulin resistance, intestinal barrier impairment, chronic low-grade inflammatory activation, abnormal bile acid metabolism regulation, and disrupted gut-pancreatic axis and gut-brain axis signaling. Using keywords such as TCM, GM, SCFAs, and T2DM, we conducted an extensive literature search across databases including PubMed, Google Scholar, and Web of Science for publications from the past decade. This systematic review examines the application of TCM in regulating the \"GM-SCFA axis\" from multiple perspectives: Chinese herbal compounds (e.g., Zuogui Jiangtang Qinggan Formula, Gegen Qinlian Decoction), Chinese patent medicines (e.g., Shouhui Tongbian Capsules, Compound Danshen Dripping Pills), single-herb Chinese medicines (e.g., Edgeworthia gardneri, Alpinia oxyphylla), single-component compounds from TCM (e.g., Cyclocarya paliurus polysaccharide, Achyranthes bidentata polysaccharide water-soluble 1), and other TCM therapies (e.g., tuina, acupuncture). This study aims to systematically explore the mechanisms by which dysregulation of the \"GM-SCFA axis\" induces T2DM while providing novel therapeutic strategies for T2DM prevention and treatment using TCM. It also seeks to establish scientific foundations for developing novel TCM intervention strategies targeting the \"GM-SCFA axis\" in T2DM management.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"35-63"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047707","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":"Flavonoids from Radix Puerariae Alleviated Alcoholic Liver Disease via PI3K/AKT Signaling Pathway.","authors":"Jiale Zhang, Miaoyu Ren, Mengran Qi, Fangyu Cui, Yangmiao Sun, Yanni Zhang, Xuanfeng Yue","doi":"10.1142/S0192415X26500345","DOIUrl":"10.1142/S0192415X26500345","url":null,"abstract":"<p><p>Alcoholic Liver Disease (ALD) represents a spectrum of hepatic disorders resulting from chronic excessive alcohol consumption. <i>Radix Puerariae</i>, the dried root of <i>Pueraria Lobata</i> (Willd.) Ohwi has been traditionally used to both counteract alcohol toxicity and protect the liver. Flavonoids, including puerarin, daidzein, and genistein, are the main bioactive components of <i>Radix Puerariae</i>. However, their specific mechanisms of action against ALD remain unclear. In this study, we therefore evaluated the hepatoprotective effects of the flavonoid from <i>Radix Puerariae</i> (FRP) using both <i>in vitro</i> and <i>in vivo</i> ALD models, and assessed the extent of pathological damage using Hematoxylin-Eosin (HE) staining. The relevant assay kits were used to measure inflammatory responses and oxidative stress-related indicators. In addition, a combination of metabolomics and network pharmacology was used to elucidate the PI3K/AKT signaling pathway as a potential mechanism of FRP-based ALD treatment. Western blotting experiments were conducted to measure the expression levels of key proteins, and the pharmacodynamic results showed that FRP reduced liver injury. Metabolomics revealed that FRP significantly regulated the levels of 73 metabolites involving the glycerophospholipid metabolism, arachidonic acid metabolism, and alpha-linolenic acid metabolism pathways. Network pharmacology results suggested that INS, AKT1, and TNF may be potential targets, and Western blot experiments showed that FRP could alleviate ALD by activating the PI3K/AKT pathway. These results indicated that FRP could exert its therapeutic effect against ALD by regulating the PI3K/AKT signaling pathway, and establish a robust application foundation for further research.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"931-953"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147730999","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}