The American journal of Chinese medicine最新文献

{"title":"Phycocyanin: Biomedical Activities and Related Mechanisms of Action.","authors":"Hongli Huang, Linhong Wang","doi":"10.1142/S0192415X26500308","DOIUrl":"10.1142/S0192415X26500308","url":null,"abstract":"<p><p>With global resources becoming increasingly strained, the development of novel sustainable resources has become particularly important. Spirulina has attracted considerable attention due to its exceptional nutritional value, abundant bioactive components, and superior environmental adaptability. A key functional component in spirulina, phycocyanin is a natural water-soluble protein pigment that exhibits diverse biological activities. In recent years, with advances in extraction and purification technologies, research on phycocyanin in the culinary, pharmaceutical, and cosmetic fields has both rapidly increased and significantly enhanced its commercial value. Despite its broad application prospects, research on its molecular mechanisms and systematic physiological effects requires further integration. This paper aims to comprehensively update the current research status of phycocyanin, systematically elucidate its biological activities as related to its anti-oxidative stress, immunomodulatory, anti-inflammatory, antitumor, and neuroprotective effects. To do so, this paper analyzes the molecular mechanisms through which phycocyanin exerts its effects, and in particular considers its regulation of key signaling pathways such as NRF2/HO-1, NF-κB, and PI3K/Akt. This review provides a detailed summary of the protective effects of phycocyanin on organs including the liver, cardiovascular system, and nervous system. It also summarizes the research progress on phycocyanin over the past 10 years, including findings related to its biological activities, functions, and related mechanisms. In conclusion, this review underscores the immense therapeutic potential of phycocyanin as a multi-target natural agent, and highlights the critical need for further clinical translation to fully harness its benefits in promoting human health and combating chronic diseases.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"827-858"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793620","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":"Quercetin Alleviates Endothelial Dysfunction in Atherosclerosis by Inhibiting Ferroptosis Through PACS2/HMOX-1 Pathway.","authors":"Hai-Jiao Long, Quan-Jun Liu, Shi-Ying Qin, Hong Xiang, Jie Ouyang, Jun-Xi Liao, Ye Tao, Jiao-Qian Huang, Shu-Hua Chen, Hong-Wei Lu","doi":"10.1142/S0192415X26500229","DOIUrl":"10.1142/S0192415X26500229","url":null,"abstract":"<p><p>Atherosclerosis is a leading cause of worldwide cardiovascular morbidity and mortality, and endothelial ferroptosis has emerged as a key mechanism in driving vascular injury. This study aimed to investigate whether quercetin (QCT), a natural dietary flavonoid with potent anti-oxidant activity, protects against atherosclerosis-associated endothelial dysfunction by modulating ferroptosis. In order to test this, ApoE[Formula: see text] mice fed a high-fat diet were treated with QCT or ferrostatin-1, and their aortic plaque burden, stability, and macrophage infiltration were then assessed. To evaluate ferroptosis, human umbilical vein endothelial cells (HUVECs) were exposed to oxidized low-density lipoprotein (Ox-LDL), with or without QCT, and their reactive oxygen species (ROS), Fe[Formula: see text] accumulation, and heme oxygenase-1 (HMOX-1) expression were measured. While functional assays examined endothelial barrier integrity and monocyte adhesion, gene modulation studies explored the role of phosphofurin acidic cluster sorting protein 2 (PACS2). QCT treatment markedly reduced plaque area, necrotic core size, and macrophage infiltration while enhancing plaque stability. <i>In vitro</i>, QCT suppressed Ox-LDL-induced ferroptosis by decreasing ROS and Fe[Formula: see text] levels and downregulating HMOX-1 to thereby restore endothelial integrity and reduce monocyte adhesion. Mechanistically, QCT restored PACS2 expression suppressed by Ox-LDL. However, PACS2 knockdown or HMOX-1 activation abrogated QCT's protective effects. These findings identify QCT as a promising dietary anti-oxidant that mitigates atherosclerosis via the PACS2-HMOX-1 ferroptosis pathway.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"603-625"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146204564","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":"Triptolide from <i>Tripterygium wilfordii</i> Suppresses Glycolysis and Induces Cuproptosis via the HK2/DLAT Signaling Pathway in Colorectal Cancer.","authors":"Hui-Hui Liang, Lu-Lu Jia, Ke Tang, Rui Xue, Rong-Rong Nie, Jian-Ning Chen, Hui-Min Xu, Xuan-Jie Qin, Shi-Kun Cai, Qin-You Tan","doi":"10.1142/S0192415X26500242","DOIUrl":"10.1142/S0192415X26500242","url":null,"abstract":"<p><p>Colorectal cancer (CRC) exhibits high mortality due to tumor cell dissemination. Surgical resection combined with chemotherapy is the primary treatment, but chemoresistance often limits its efficacy against metastasis. Cuproptosis, a novel cell death mechanism regulating mitochondrial and lipid metabolism, may suppress metastasis by inhibiting cellular metabolism. Triptolide (TP), a potential antitumor agent derived from <i>Tripterygium wilfordii</i>, can reverse chemoresistance. This study investigated the link between TP's anti-CRC effects and cuproptosis. Cell Counting Kit-8 (CCK-8), colony formation, wound healing, and transwell migration/invasion assays demonstrated that TP inhibited the proliferation, migration, and invasion of SW480 and HCT116 cells in a dose-dependent manner. Bioinformatic analysis implicated glycolysis and cuproptosis in TP's anti-CRC action. Subsequent validation via glucose metabolism assays, reactive oxygen species (ROS) detection, JC-1 staining, copper ion measurement, morphological observation, qRT-PCR, and Western blotting confirmed that TP had a significant effect in both suppressing glycolysis and inducing cuproptosis in SW480 and HCT116 cells. In addition, <i>in vivo</i> studies have shown that TP significantly inhibits tumor growth and promotes copper accumulation within tumors. Furthermore, hematoxylin-eosin (H&E) staining and biochemical analysis have indicated that it has no obvious liver or kidney toxicity. These results suggest that TP may both inhibit the glycolysis of CRC and induce cuprotosis via the Hexokinase 2 (HK2)/Dihydrolipoamide S-acetyltransferase (DLAT) pathway. Future research should systematically verify its effectiveness and safety through <i>in vivo</i> studies and clinical trials to promote the application of TP in CRC treatment.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"661-683"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146222536","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 for the Treatment of Inflammatory Bowel Disease: From Mechanism to Clinic.","authors":"Yushan Wu, Jiangmei Pang, Jiaxin Li, Mingshan Jiang, Hao Lin, Hu Zhang","doi":"10.1142/S0192415X26500217","DOIUrl":"10.1142/S0192415X26500217","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) is characterized by chronic symptoms, frequent relapses, and an increased risk of complications such as colorectal cancer. These qualities significantly impair patients' quality of life, and while various treatment options are available, they are often limited by inconsistent responses, unclear long-term safety, considerable individual variability, restricted drug accessibility, high costs, and the complexity of combination therapies. Such challenges thus highlight the urgent need for novel, safer, and more effective treatments. Curcumin, a natural compound with diverse biological activities, shows promise in IBD management. This review discusses the mechanisms of curcumin in IBD, highlights its multi-target regulation of both signaling pathways and various immune cell populations, and emphasizes its potent anti-oxidant and anti-inflammatory effects. In addition, curcumin has been shown to strengthen intestinal barrier function and modulate the intestinal microbiota. While clinical studies indicate that curcumin can improve symptoms, endoscopic findings, and laboratory markers in IBD patients, its low bioavailability remains a challenge. Recent research has focused on enhancing curcumin's stability, targeting, and bioavailability to optimize its therapeutic potential. Insights from curcumin's use in other diseases further support its potential in IBD treatment. Despite these promising findings, further high-quality clinical trials and the development of novel curcumin formulations are necessary to enable its practical clinical application in IBD.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"573-602"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147313698","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":"Nobiletin Ameliorated the Development of Diabetic Kidney Disease via Modulating Ferroptosis and Epithelial-Mesenchymal Transition Involving Gut-Kidney Axis.","authors":"Tingting Zhao, Chuyun Zhao, Qian Xiang, Xi Zhang, Kin-Fong Hong, Peiyu Liu, Zhongyan Sun, Yadi Liu, Ruiting Huang, Yiran Li, Hio-Fai Cheong, Yuwei Wu, Yingqiu Mo, Yiduo Xu, Yingxi Zhao, Qiruo Huang, Ying Xie, Youhua Xu","doi":"10.1142/S0192415X26500114","DOIUrl":"10.1142/S0192415X26500114","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD) is one of the most common microvascular complications associated with diabetes mellitus. However, the existing treatment approaches, aimed at delaying the onset of DKD, exhibit limited efficacy. The flavonoid nobiletin has demonstrated substantial lipid-lowering and insulin-sensitizing effects in mice exhibiting metabolic dysfunction, but the therapeutic potential and mechanism of nobiletin in the context of DKD remains to be comprehensively elucidated. In this study, the active components of polymethoxylated flavonoids (PMFs) were identified via UPLC. A DKD rat model was established through a high-fat diet and the administration of streptozotocin via intraperitoneal injection. The effect and mechanism of nobiletin on DKD was evaluated by histological, biochemical, molecular, and multi-omics analysis. We found that treatment with PMFs and nobiletin inhibited ferroptosis and EMT in high glucose and insulin-induced models, protected the glomerular filtration barrier integrity, and concurrently suppressed ROS, Fe[Formula: see text], and MDA while increasing the GSH level. Animal experiments indicated that nobiletin treatment markedly impeded the progression of DKD and alleviated both EMT and endothelial dysfunction. Moreover, nobiletin significantly preserved the integrity of the intestinal barrier and enriched the diversity of gut microbiota. In conclusion, our findings indicate that nobiletin could attenuate DKD and concomitantly limit ferroptosis and EMT, and that the gut-kidney axis played an important role in its effects.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"303-328"},"PeriodicalIF":5.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047722","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":"https://doi.org/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":"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":"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":"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}