Dan Wu, Ping Shi, Lian-Hua Tang, Xiao-Mei Song, Juan Deng, Hong Guo, Fei Yin
{"title":"Celastrol Alleviates Intestinal Epithelial Permeability by Inhibiting Ferroptosis through PI3K/Akt/FOXO1/HO-1 Signaling Pathway.","authors":"Dan Wu, Ping Shi, Lian-Hua Tang, Xiao-Mei Song, Juan Deng, Hong Guo, Fei Yin","doi":"10.1142/S0192415X25500466","DOIUrl":"https://doi.org/10.1142/S0192415X25500466","url":null,"abstract":"<p><p>Ulcerative colitis (UC) is a recurrent inflammatory intestinal disorder characterized by systemic inflammatory response, abnormal intestinal epithelial cell death, and damage to the intestinal mucosal barrier. This study aimed to explore the role of celastrol in ferroptosis and intestinal epithelial barrier permeability. The results demonstrated that celastrol significantly inhibited ferroptosis in RSL3-induced intestinal epithelial cells by regulating the expression of ferroptosis-related proteins. Concurrently, celastrol dramatically improved the permeability of the intestinal epithelial monolayer by increasing the expression of tight junction proteins including ZO-1, occludin, and claudin-1. Moreover, celastrol markedly attenuated the effect of RSL3 on the phosphorylation of Akt and FOXO1. LY294002, a PI3K inhibitor, significantly inhibited the role of celastrol in the expression of ferroptosis-related and intestinal tight junction proteins. <i>In vivo</i>, celastrol administration not only significantly ameliorated dextran sulfate sodium (DSS)-induced colitis by preventing neutrophil infiltration, but also ameliorated intestinal mucosa damage, and colon shortening. Celastrol administration was also found to reduce the expression of ferroptosis-related proteins prevent the infiltration of fluorescein isothiocyanate-dextran (FITC-dextran) and increase the levels of tight junction proteins. Collectively, these findings suggest that due to its effects on ferroptosis and tight junctions in intestinal epithelial cells, celastrol may be a compound with significant promise in the prevention and treatment of UC.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 4","pages":"1207-1224"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532186","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}
Qing Nian, Ziqiang Liu, Jinhao Zeng, Duo Cai, Yanna Zhang
{"title":"Targeting Myeloperoxidase in Disease Pathogenesis: Emerging Roles of Natural Products in Therapeutic Modulation.","authors":"Qing Nian, Ziqiang Liu, Jinhao Zeng, Duo Cai, Yanna Zhang","doi":"10.1142/S0192415X25500740","DOIUrl":"10.1142/S0192415X25500740","url":null,"abstract":"<p><p>Myeloperoxidase (MPO) is a heme-containing enzyme that regulates inflammation and oxidative stress under normal physiological conditions, but when dysregulated, it contributes to the development and progression of cardiovascular, immune-related, and malignant diseases. While its pathological roles have been widely described, the therapeutic applications of targeting this enzyme remain insufficiently explored. Natural compounds, including polyphenols, flavonoids, and traditional herbal formulations, possess anti-oxidant and anti-inflammatory properties that attenuate oxidative stress and modulate MPO activity. This review explores the molecular pathways through which dysregulated MPO activity promotes disease and compiles a categorized overview of natural products and traditional Chinese medicines capable of influencing MPO function. These findings provide a framework for therapeutic discovery, thus enabling target validation and the development of novel interventions across diverse inflammatory and degenerative conditions.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1983-2019"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144984569","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":"The Role of Traditional Chinese Medicine in the Management of Nonalcoholic Fatty Liver Disease: Targeting Gut Microbiome.","authors":"Yifan Zhang, Hongkun Li, Na Jiang, Qingjing Ru","doi":"10.1142/S0192415X25500788","DOIUrl":"10.1142/S0192415X25500788","url":null,"abstract":"<p><p>The incidence of non-alcoholic fatty liver disease (NAFLD) has increased and become a serious global public health problem in recent years. The currently generally used clinical treatments have disadvantages such as side effects, limitations, and poor patient compliance. Traditional Chinese medicine (TCM) has a pharmacological effect with multiple components, multiple targets, and multiple pathways, emphasizing a \"holistic concept\" and \"differential diagnosis and treatment,\" which is compatible with the complex pathogenesis of GM and NAFLD. Previous studies have demonstrated a close relationship between the gut microbiome (GM) and the occurrence and progression of NAFLD. However, the mechanisms between GM and NAFLD are complex. This paper not only analyzes the relationship between the GM and the pathogenesis of NAFLD but also discusses in detail how various TCM active metabolites and Chinese herbal formulas could exert a therapeutic effect on NAFLD by regulating the GM and its metabolites. Furthermore, this paper innovatively explores how TCM regulates the abundance of five major bacterial phyla, and their representative genera, to improve the pathogenesis of NAFLD. In summary, this review article proposes innovative ideas and options for the prevention and treatment of NAFLD with focus on GM regulation, and provides a theoretical basis for the development of new drugs from traditional Chinese medicine.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"2103-2136"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031672","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":"Ameliorative Effect of Glycyrrhizic Acid on Diosbulbin B-Induced Liver Injury and Its Mechanism.","authors":"Xin Wang, Lei-Lei Shi, Yu-Han Zhang, Hong-Zhe Zhu, Shan-Shan Cao, Yong Shi, Hui-Zi Shangguan, Ji-Ping Liu, Yun-Dong Xie","doi":"10.1142/S0192415X25500120","DOIUrl":"10.1142/S0192415X25500120","url":null,"abstract":"<p><p>This study aimed to clarify the protective effect of Glycyrrhizic acid (GL) against Diosbulbin B (DB) - induced liver injury in mice and investigate its mechanisms of action. A liver injury DB was established in mice through the oral administration of DB for 15 days. At the same time, GL was administered to the mice for treatment. After the experiment, the pharmacodynamics and mechanisms of GL in ameliorating DB-induced liver injury were explored using biochemical indexes, non-targeted metabolomics, targeted metabolomics, Western blotting analysis of protein expression, 16S rDNA sequencing, and Spearman correlation analysis. The results show reduced liver function indices and improved DB-induced hepatic pathological changes. It also attenuated DB-induced hepatic inflammation and oxidative stress. Hepatic metabolomics revealed that GL regulated ABC transporters and bile secretion. Targeted bile acid (BA) metabolomics and Western blotting demonstrated that GL improved DB-induced reduction in BA efflux by regulating FXR-mediated efflux transporters. Furthermore, analysis of 16S rDNA gene sequencing revealed that GL effectively restored the relative abundance of beneficial bacteria, reduced the relative abundance of harmful bacteria, and reinstated the structure of the intestinal flora. Additionally, correlation analyses between BA and intestinal flora indicated that <i>Firmicutes, Bacteroidota</i>, TDGA, DGA, UDGA, GDGA, THDGA, and HDGA could serve as major markers for DB-induced liver injury. In conclusion, GL significantly improved DB-induced liver injury by increasing the expression of Nrf2/FXR-BSEP/MRP2/P-gp/UGT1A1, promoting BA efflux, regulating intestinal flora, and alleviating inflammation and oxidative stress.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"309-335"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019335","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}
Huate Xu, Jinhui Zhu, Xiangyun Lin, Chao Chen, Jinhua Tao
{"title":"A Comprehensive Review of Traditional Chinese Medicine in the Management of Ulcerative Colitis.","authors":"Huate Xu, Jinhui Zhu, Xiangyun Lin, Chao Chen, Jinhua Tao","doi":"10.1142/S0192415X2550017X","DOIUrl":"10.1142/S0192415X2550017X","url":null,"abstract":"<p><p>Ulcerative colitis (UC) is a chronic, nonspecific inflammatory disorder characterized by symptoms such as abdominal pain, diarrhea, hematochezia, and urgency during defecation. While the primary site of involvement is the colon, UC can extend to encompass the entire rectum and colon. The causes and development mechanisms of UC are still not well understood; nonetheless, it is currently held that factors including environmental influences, genetic predispositions, intestinal mucosal integrity, gut microbiota composition, and immune dysregulation contribute to its development. Dysregulated immune responses are pivotal in the pathophysiology of UC, and these aberrant responses are considered key contributors to the disease onset. In patients with UC, immune cells become hyperactive and erroneously target normal intestinal tissue, resulting in inflammatory cascades and damage to the intestinal mucosa. The therapeutic strategies currently employed for UC include immunosuppressive agents such as aminosalicylates and corticosteroids. However, these treatments often prove costly and carry significant adverse effects - imposing a considerable burden on patients. Traditional Chinese Medicine (TCM) has attracted worldwide attention because of its multi-target approach, minimal side effects, cost-effectiveness, and favorable efficacy profiles. In this review, the ways in which TCM modulates inflammatory responses in the treatment of ulcerative colitis have been outlined. Research into TCM modalities for modulating inflammatory pathways in the treatment of UC, which has yielded promising advancements, including individual herbs, herbal formulations, and their derivatives, has been summarized. TCM has been utilized to treat UC and the immune system plays a key role in regulating intestinal homeostasis. It is imperative to facilitate large-scale evidence-based medical research and promote the clinical application of TCM in the management of UC.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"435-473"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598679","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":"Electroacupuncture Preconditioning Attenuates Myocardial Ischemia-Reperfusion Injury in Rats Partially Through Nrf2-Mediated Reduction of Oxidative Stress and Pyroptosis.","authors":"Xuefeng Xia, Yaping Ding, Chunmei Zhou, Hanyu Zhang, Xinran Yang, Chuchu Shen, Senlei Xu, Hongru Zhang, Yihuang Gu, Hua Bai","doi":"10.1142/S0192415X25500132","DOIUrl":"10.1142/S0192415X25500132","url":null,"abstract":"<p><p>Oxidative stress and pyroptosis have been established as key contributors to myocardial ischemia-reperfusion injury (MIRI). While previous studies reported that electroacupuncture (EA) preconditioning exerted cardioprotective effects, the underlying mechanisms remain elusive. Thus, this study aimed to investigate the effects of EA preconditioning on oxidative stress and pyroptosis in MIRI rats, and explore the role of nuclear factor E2-associated factor 2 (Nrf2) throughout that process. A MIRI model was constructed by ligating the left anterior descending coronary artery for 30 min, followed by 4 h of reperfusion in rats. Prior to modeling, rats were subjected to EA at the Neiguan Point for three days. Furthermore, ML385, a Nrf2 inhibitor, was administered in order to examine the role of Nrf2 in regulating oxidative stress and pyroptosis following EA preconditioning. The results revealed that EA preconditioning improved left ventricular function after MIRI and reduced both the myocardial infarction area and cTnT levels. Meanwhile, EA preconditioning alleviated MIRI-induced oxidative stress and pyroptosis, as evidenced by the downregulation of ROS, MDA, NF-κB p65, caspase-1, IL-1β, and GSDMD-N, and the upregulation of SOD and HO-1. Mechanistically, EA up-regulated enhanced the expression of Nrf2. However, its cardioprotective effects and ability to attenuate oxidative stress and pyroptosis were suppressed by the inhibition of Nrf2. Taken together, our study indicated that EA preconditioning attenuated MIRI in rats by mitigating oxidative stress and pyroptosis, with Nrf2 playing a vital role in this protective mechanism.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"337-352"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143665652","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":"Application of Large Language Models in Traditional Chinese Medicine: A State-of-the-Art Review.","authors":"Dilireba Shataer, Siyu Cao, Xin Liu, Kailibinuer Aierken, Pronaya Bhattacharya, Anurag Sinha, Haipeng Liu","doi":"10.1142/S0192415X25500375","DOIUrl":"https://doi.org/10.1142/S0192415X25500375","url":null,"abstract":"<p><p>Large language models (LLMs) are reshaping the landscape of Traditional Chinese Medicine (TCM). This review covers the latest applications of LLMs in TCM, including literature analysis, data mining, TCM knowledge management, diagnosis simulation and clinical decision making. LLMs can analyze large quantities of TCM literature and medical records to extract critical information, classify prescriptions, and build TCM knowledge maps to help researchers quickly grasp state-of-the-art and future research trends. LLMs can provide initial diagnostic recommendations by analyzing textual information such as a patient's symptom description and medical history, enabling the optimization of TCM therapy and the training of TCM practitioners. Compared with traditional tools, LLMs can significantly improve the efficiency and accuracy of bibliographic analysis and TCM prescription classification, and offer new potential for data-driven standardized TCM diagnosis. However, challenges remain, including the standardization of TCM terminology and data formats, integration of different data sources, timely knowledge updates, and the interpretability and credibility of results generated by LLMs. Future research on standardized templates for patient symptom description, multimodal data fusion techniques, and real-time knowledge update systems is warranted to improve the transparency and interpretability of LLMs. This review highlights the potential of LLMs to modernize TCM research and practice, providing an up-to-date reference for data scientists, biomedical engineers, and TCM practitioners.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 4","pages":"973-997"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532184","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}
Jun-Jie Huang, Rui-Gang Zhou, Jun Chen, Wei-Long Peng, Cheng-Long Yu, Ming-Jiang Liu, Ruo-Nan Bo, Shao-Jie Yin, Jin-Gui Li
{"title":"Eugenol Exerted Significant Anti-Oxidant and Anti-Inflammatory Effects on Experimental Colitis via Directly Acting on PPAR-[Formula: see text].","authors":"Jun-Jie Huang, Rui-Gang Zhou, Jun Chen, Wei-Long Peng, Cheng-Long Yu, Ming-Jiang Liu, Ruo-Nan Bo, Shao-Jie Yin, Jin-Gui Li","doi":"10.1142/S0192415X25500727","DOIUrl":"10.1142/S0192415X25500727","url":null,"abstract":"<p><p>In a previous study, Eugenol (EU) has been demonstrated to alleviate DSS-induced experimental colitis, due to its anti-inflammatory, anti-oxidant, and immune regulatory efficacy, but its underlying molecular mechanism remains unknown. In this study, EU applications were combined with peroxisome proliferator-activated receptor-[Formula: see text] (PPAR-[Formula: see text]) agonist (rosiglitazone) and inhibitor (GW9662) in order to clarify the role of PPAR-[Formula: see text] in EU against UC by testing NF-κB and Nrf2 signaling pathway activation and the salient features of colitis. The binding activity and adjusting effect of EU on inflammation and oxidative stress were further investigated <i>in vitro</i>. Similar to rosiglitazone, the results illustrated that EU remarkably reversed DSS-induced weight loss, reversed colonic shrinkage and integrity damage, and inhibited the DAI scores increase, excessive inflammatory response, and oxidative stress. However, the combination with GW9662 noticeably restrained the protective effect on mice. Additionally, molecular docking and a surface plasmon resonance assay evidenced the direct binding activity of EU with PPAR-[Formula: see text]. EU's anti-oxidant and anti-inflammation bioactivities were evidenced again <i>in vitro</i>. Overall, the above results further demonstrated the molecular mechanism of EU's defensive effect, which is directly dependent on PPAR-[Formula: see text] activation, on experimental colitis. Therefore, this study may facilitate a better understanding of EU's protective action against UC.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1933-1949"},"PeriodicalIF":5.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755538","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":"Astragaloside IV: A Promising Drug to Prevent the Transition from Colitis to Colorectal Cancer.","authors":"Jiayu Ran, Yanling Ai, Jingxin Ni, Yuanhao Zhang, Jie Chen, Tingyao Wang, Jia Ma, Jijun Zheng, Ruilin Li, Xiao Ma, Yueqiang Wen, Jinhao Zeng","doi":"10.1142/S0192415X25500405","DOIUrl":"10.1142/S0192415X25500405","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a major threat to health worldwide, partly due to the lack of effective treatments targeting the transition from inflammatory bowel disease (IBD) to malignancy. Astragaloside IV (AS-IV) is a major bioactive component from the traditional herb <i>Astragalus membranaceus</i>, and it has strong immunomodulatory and gastrointestinal protective effects. In this review, we evaluate the therapeutic potential and mechanisms of AS-IV in addressing the three hallmark pathological phases of colorectal cancer development: IBD-related inflammation, the transition from inflammation to cancer, and IBD-associated colorectal cancer (IBD-CRC). During the inflammatory phase, AS-IV promotes M2 macrophage polarization, reducing mucosal inflammation and repairing the intestinal barrier. In the transition from inflammation to cancer, AS-IV prevents IBD-CRC transition by targeting immune signaling pathways (e.g., NF-κB and PPAR[Formula: see text] signaling pathways), gut microbiota, and oxidative stress. At the IBD-CRC stage, AS-IV can promote the polarization of M1 macrophages, thereby suppressing tumor growth, inducing apoptosis, inhibiting metastasis, and enhancing chemosensitivity. These findings highlight the potential of AS-IV to bidirectionally modulate the M1/M2 macrophage ratio and its role in the prevention and treatment of IBD-CRC. The multi-target therapeutic effects of AS-IV at various stages of IBD also provide new strategies to guide future drug development.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1065-1091"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328278","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":"Sanguinarine Inhibits Gastric Cancer Progression by Targeting the NOS2/SOD1 Axis to Promote Ferroptosis.","authors":"Zhaotian Feng, Muhua Luan, Wenshuai Zhu, Yuanxin Xing, Xiaoli Ma, Yunshan Wang, Yanfei Jia","doi":"10.1142/S0192415X25500594","DOIUrl":"10.1142/S0192415X25500594","url":null,"abstract":"<p><p>Ferroptosis, an iron-dependent form of non-apoptotic cell death, has emerged as a critical process in cancer therapy. Sanguinarine chloride (S.C), an alkaloid that stimulates apoptosis by activating reactive oxygen species (ROS), has demonstrated significant anticancer potential, but its role in modulating ferroptosis remains unclear. The aim of the present study was to elucidate the effects of S.C on ferroptosis in gastric cancer (GC) progression and its mechanism. Here, we determined cell viability by CCK-8 and revealed that the most potent drug, S.C, which is a small molecule compound in the ferroptosis library, had the strongest killing effect on GC cells. S.C could trigger ferroptosis in GC cells by inhibiting glutathione levels through promoting malondialdehyde production and ROS accumulation. Interestingly, S.C was found to function as a pro-ferroptotic death by interacting with NOS2 through network pharmacological docking. Mechanistically, we observed the deacetylase SIRT1 to regulate the acetylation level of NOS2 and thus affect the expression of NOS2. In addition, S.C regulates the downregulation of SLC7A11 and GPX4 through the SIRT1/NOS2/SOD1 pathway, and thereby induces ferroptosis. <i>In vivo</i> experiments showed that S.C treatment significantly inhibited subcutaneous tumor growth in BALB/c nude mice. This was significantly rescued by injection of a ferroptosis rescue agent (AA9). Taken together, these findings demonstrate that S.C works through the SIRT1/NOS2/SOD1 pathway and suggest that targeting SLC7A11/GPX4 to cause ferroptosis in cancer cells has potential as an anticancer therapy.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1545-1571"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144644471","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}