The American journal of Chinese medicine最新文献

{"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":"https://doi.org/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":"1-27"},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","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}

{"title":"Quercetin Ameliorates Learning and Memory in OVX/D-gal-Induced Alzheimer's Disease in Rats by Inhibiting Neuroinflammation via cGAS-STING Signal Pathway.","authors":"Xin Zhang, Meng-Fan Ma, Rui Zong, Hong-Bin Liu, Tian-Xu Wang, Ci Liu, Yong-Yuan Cui, Liang-Jing Liu, Miao-Miao Wu, Li-Xia Shen","doi":"10.1142/S0192415X25500569","DOIUrl":"https://doi.org/10.1142/S0192415X25500569","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is an age-related degenerative disorder of the central nervous system. Neuroinflammation is considered a key factor in its etiology and progression. AD is more prevalent in women than men and may be related to postmenopausal hormone deficiency. This study constructed an AD rat model by bilateral ovariectomy (OVX) and intraperitoneal injection of D-galactose (D-gal) and an <i>in vitro</i> AD cell model was induced in PC12 cells using lipopolysaccharide (LPS). The Morris water maze test was employed to assess the impact of quercetin (Que) on learning and memory in OVX/D-gal rats. Immunohistochemistry was utilized to assess the impact of Que on the expression of Aβ protein, p-tau protein, GFAP, and Iba1 in the hippocampus of OVX/D-gal rats. Nissl staining was performed to examine hippocampal pathological damage. ELISA was conducted to measure serum estrogen levels and the release of inflammatory cytokines, specifically TNF-α and IL-1β, in the hippocampus of OVX/D-gal rats. HE staining was utilized to evaluate uterine pathological alterations in OVX/D-gal rats. Cell viability was assessed using the CCK-8 assay to determine the protective effect of quercetin on LPS-induced PC12 cells. Western Blot analysis was conducted to evaluate the expression levels of estrogen receptors and the proteins associated with the cGAS-STING pathway in both <i>in vitro</i> and <i>in vivo</i> models. Protein-protein docking studies were performed to investigate the binding affinity between the estrogen receptor and proteins involved in the cGAS-STING signaling pathway. Results demonstrated that Que enhanced learning and memory capabilities in OVX/D-gal rats, alleviated hippocampal pathological damage, reduced the expression of Aβ, p-tau, GFAP, and Iba1, and inhibited the release of inflammatory factors. Additionally, Que activated estrogen receptor expression and increased serum estrogen levels without exacerbating uterine lesions. Furthermore, Que activated the estrogen receptor in LPS-induced PC12 cells, which inhibited the release of IL-6 and exerted neuroprotective effects. Que also suppressed the expression of proteins associated with the cGAS-STING pathway both <i>in vitro</i> and <i>in vivo</i>. Estrogen receptors exhibited strong binding affinity with cGAS-STING pathway proteins. In conclusion, Que can inhibit neuroinflammation <i>in vitro</i> and <i>in vivo</i>, enhance learning and memory in OVX/D-gal rats, and exert neuroprotective effects. The underlying mechanism may involve the inhibition of the cGAS-STING signaling pathway, and the estrogen receptor potentially influences this pathway directly or indirectly.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-23"},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144644470","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":"SNHG5 Upregulated by Dexmedetomidine Alleviates Myocardial Ischemia/Reperfusion Injury Through LIN28A-Mediated BCAT1 mRNA Stabilization and Autophagy Enhancement.","authors":"Jingjia Yu, Fei Ye, Wenzhi Luo, Xu Deng","doi":"10.1142/S0192415X25500442","DOIUrl":"https://doi.org/10.1142/S0192415X25500442","url":null,"abstract":"<p><p>SNHG5 serves as a key factor in regulating various cancers, and Dexmedetomidine (Dex) protects against myocardial ischemia/reperfusion (I/R) injury. However, the role of SNHG5 in Dex-mediated protection during myocardial I/R remains uninvestigated. In this study, models of rat myocardial I/R injury and hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury were generated. The infarct size, histological changes and apoptosis in heart tissues were evaluated by TTC, HE, and TUNEL staining. CCK-8, flow cytometry and immunofluorescence were employed to assess cell viability, apoptosis and autophagosome-lysosome fusion in H9c2 cells. The associations among SNHG5, LIN28A and BCAT1 mRNA were detected by RNA pull-down, RIP, and RNA fluorescence <i>in situ</i> hybridization (FISH) assays. Western Blot, qRT-PCR and immunohistochemistry were employed to detect the expression of key molecules. Our results revealed that Dex ameliorated myocardial I/R injury and H/R-induced impairments in H9c2 cells by enhancing autophagy. Moreover, Dex led to a rebound of SNHG5 in the heart tissues of I/R rats and H/R-treated H9c2 cells, and functional studies revealed that Dex protected against cardiac impairments through SNHG5-dependent autophagy <i>in vitro</i> and <i>in vivo</i>. Furthermore, SNHG5 alleviated H/R-induced impairments by recruiting LIN28A protein, which was subsequently bound to BCAT1 mRNA and maintained its stability. In conclusion, our findings demonstrated that SNHG5, when upregulated by Dex, alleviated myocardial I/R injury through LIN28A-mediated BCAT1 mRNA stabilization and autophagy enhancement.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-22"},"PeriodicalIF":0.0,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621596","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":"Puerarin Attenuates Myocardial Ischemia-Reperfusion Damage by Targeting Ferroptosis through 14-3-3η Modulation.","authors":"YaMei Qiao, SongQing Lai, YaRu Wang, FaJia Hu, Yue Liu, FeiXiang Zhai, ZeYu Zhang, Dan Liu, Huang Huang","doi":"10.1142/S0192415X25500570","DOIUrl":"https://doi.org/10.1142/S0192415X25500570","url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion (I/R) injury continues to be a significant clinical challenge, and ferroptosis has been identified as a major contributing factor to its development. Puerarin (Pue), an isoflavone derived from <i>Pueraria lobata</i>, has demonstrated promising cardioprotective effects, although the mechanisms involved are not fully elucidated. This study explores Pue's ability to attenuate myocardial I/R damage through the modulation of ferroptosis, specifically focusing on the role of the 14-3-3η protein. Network pharmacology identified 356 potential targets for Pue, with 25 genes overlapping between myocardial I/R injury and ferroptosis pathways. Molecular docking analysis revealed a strong interaction between Pue and 14-3-3η, suggesting a mechanistic link. <i>In vitro</i> studies using H9c2 cardiomyocytes showed that Pue pretreatment significantly improved cell viability and reduced lactate dehydrogenase (LDH) release under conditions of anoxia/reoxygenation (A/R). Pue's inhibition of ferroptosis was evidenced by reduced iron accumulation, decreased malondialdehyde (MDA) levels, lowered reactive oxygen species (ROS), and boosted anti-oxidant defenses. Central to these protective effects was the upregulation of 14-3-3η, and knockdown experiments confirmed its pivotal role in ferroptosis regulation. Furthermore, Pue preserved mitochondrial function by stabilizing mitochondrial membrane potential, limiting mitochondrial permeability transition pore (mPTP) opening, and improving mitochondrial energy metabolism and structural integrity. These activities were all mediated by 14-3-3η. <i>In vivo</i>, Pue administration in a rat I/R model significantly reduced myocardial injury markers and improved cardiac function, and its effects were reversed when 14-3-3η expression was downregulated. This study provides compelling evidence that Pue mitigates myocardial I/R injury by inhibiting ferroptosis through 14-3-3η modulation, and presents a novel therapeutic avenue for cardioprotection.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-20"},"PeriodicalIF":0.0,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621582","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":"Plant-Derived Natural Products Ameliorating Hypertension via Signaling Pathways: A Review.","authors":"Yushen Feng, Juan Zhou, Min Zhong, Didi Ma, Jian Mao, Fugui Liu, Chengxi Jiang, Xiaodan Wu, Lan Jiang","doi":"10.1142/S0192415X2550051X","DOIUrl":"https://doi.org/10.1142/S0192415X2550051X","url":null,"abstract":"<p><p>More than one billion people worldwide suffer from hypertension, and essential arterial hypertension is in particular a major risk factor for cardiovascular diseases. These conditions can lead to complications such as stroke, renal failure, cardiac hypertrophy, and heart failure. Despite extensive research on various antihypertensive drugs, an increasing number of people are unable to effectively control their hypertension. Further optimization of their treatment is required. Given the pathogenesis of hypertension, natural products (NPs) have emerged as a promising source of potential antihypertensive agents. NPs can prevent the development of hypertension by targeting oxidative stress, inflammation, vascular remodeling, and neurohormonal pathways. These targets provide the foundation for the application of NPs in clinical treatment. This review assesses NPs with potential antihypertensive activities published between 2019 and 2024. A total of 70 unique NPs were identified through PubMed and Web of Science. Seventy unique NPs were categorized into flavonoids (20 compounds), terpenoids (24 compounds), alkaloids (17 compounds), and plant-derived extracts (9 species). These products were classified according to their structural frameworks, and their bioactivities were briefly summarized. Future research should prioritize NPs with dual anti-oxidant/anti-inflammatory properties for clinical experiments, advanced delivery systems for improved bioavailability, and interdisciplinary approaches integrating synthetic biology for scalable production.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-45"},"PeriodicalIF":0.0,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586024","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":"Mast Cells in Acupoint Sensitization: Mechanisms and Research Advances.","authors":"Ran Li, Miao Liu, Yueming Lv, Fujie Jing","doi":"10.1142/S0192415X25500491","DOIUrl":"https://doi.org/10.1142/S0192415X25500491","url":null,"abstract":"<p><p>Acupoint sensitization is characterized by a dynamic transition from a \"resting state\" to an \"activated state\". Research in this area holds significant implications not only for clinical acupoint selection but also for disease diagnosis. However, the biological mechanisms and material basis underlying this process require further investigation. In recent years, mast cells have been recognized as a key cellular foundation and an objective indicator of acupoint sensitization. When mechanical signals are transmitted to the subcutaneous tissue, mast cell aggregation and degranulation are induced. This leads to subsequent effects on the surrounding tissues, including blood vessels, muscles, and nerve endings, and thereby mediates the acupuncture effect. Evidence suggests that mast cells not only initiate acupuncture effects but also, through their released substances, reflect the dynamic and functional characteristics of acupoint sensitization. These cells also contribute to both central and peripheral sensitization processes. Despite recent advancements, several challenges remain in the study of acupoint sensitization, including the lack of dynamic monitoring methods, inconsistent indicators for measuring sensitization intensity, and an uncertainty regarding the potential of neurotransmitter-independent sensitization processes. This study provides an overview of mast cells and their role in the mechanism of acupoint sensitization, thereby aiming to establish a comprehensive network linking the central and peripheral systems to the neuroendocrine-immune system. The study aims to offer insights that will facilitate further exploration of the biological significance of acupoint sensitization and promote more in-depth research.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-20"},"PeriodicalIF":0.0,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586023","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":"CORRIGENDUM: <i>Gardenia jasminoides</i> Extract GJ-4 Aleviates Memory Defciency of Vascular Dementia in Rats through PERK-Mediated Endoplasmic Reticulum Stress Pathway.","authors":"Fang-Yu Yuan, Cheng Ju, Cai-Xia Zang, Hui Liu, Mei-Yu Shang, Jing-Wen Ning, Yang Yang, Jing-Wei Ma, Gen Li, Yang Yu, Xin-Sheng Yao, Xiu-Qi Bao, Dan Zhang","doi":"10.1142/S0192415X25920016","DOIUrl":"https://doi.org/10.1142/S0192415X25920016","url":null,"abstract":"","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586022","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":"Geniposide Suppresses Tumor Progression Through DUOX1-Mediated Ferroptosis in Hepatocellular Carcinoma.","authors":"Mei Luo, Yuelian Wang, Xiaodong Liu, Lin Liu, Li Zhu, Guo Chen, Qing Ye, Chengshi He, Xujue Xiao, Jike Li","doi":"10.1142/S0192415X25500600","DOIUrl":"https://doi.org/10.1142/S0192415X25500600","url":null,"abstract":"<p><p>Among the spectrum of digestive system cancers, hepatocellular carcinoma (HCC) poses a particularly formidable challenge due to its poor prognosis. Geniposide, an iridoid glucoside extracted from the fruit of <i>Gardenia jasminoides</i> Ellis, exhibits a diverse array of biological activities. The goal of this study is to delineate the specific roles and underlying mechanisms of geniposide on the progression of HCC. Cell viability, apoptosis and migration of Huh7 and HepG2 cells were, respectively, assessed via CCK-8, flow cytometry and trans-well assays. The level of reactive oxygen species (ROS) was assessed with a dihydroethidium (DHE) probe. The measurement of mitochondrial membrane potential (MMP) was conducted using JC-1 staining. Ferroptosis-related markers were evaluated by Western Blot assay. Transcriptome sequencing was performed in HCC cells both treated and untreated with geniposide. <i>In vivo</i> experiments were applied with the subcutaneous xenograft tumor model. <i>In vitro</i> experiments revealed that geniposide exerted a concentration-dependent suppression on cell viability and migration, concurrently eliciting apoptosis in HCC cells. Ferroptosis was identified as the main form of geniposide-induced cell death in HCC. Geniposide promoted the iron ions levels, ROS accumulation, and the expression of ferroptosis markers, which were partially reversed by the addition of deferoxamine (DFO, ferroptosis inhibitor). Intersection analysis was applied between upregulated genes of HCC cells and ferroptosis-related genes. DUOX1 was proven to be involved in geniposide-mediated roles in HCC. <i>In vivo</i> experiments further clarified the suppressive effects of geniposide on tumors. Geniposide treatment increased intracellular iron ions and induced ferroptosis in HCC. Geniposide attenuated tumor progression and oxidative stress via DUOX1-mediated ferroptosis.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-17"},"PeriodicalIF":0.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144577485","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":"Advances and Perspectives on the Anti-Fibrotic Mechanisms of the Quercetin.","authors":"Xiaoqin Liu, Qingzhi Liang, Yufeng Qin, Zhengtao Chen, Rensong Yue","doi":"10.1142/S0192415X25500545","DOIUrl":"https://doi.org/10.1142/S0192415X25500545","url":null,"abstract":"<p><p>Fibrosis is a pathological process that affects multiple tissues and organs and a significant contributor to mortality, particularly in developed countries. Dietary flavonoids, especially quercetin (QUR), have emerged as key bioactive compounds with protective effects on vital organs such as the liver, heart, lungs, and kidneys. As a prominent focus in natural product research, QUR exhibits diverse anti-fibrotic mechanisms across various fibrotic conditions, including modulation of the TGF-[Formula: see text], NF-[Formula: see text]B, Nrf2, and AREG/EGFR signaling pathways. This review consolidates current knowledge on QUR and its derivatives, covering their anti-fibrotic mechanisms, drug interactions, pharmacokinetics, safety, and toxicological profiles. It offers insights for developing novel QUR-based formulations. Our findings highlight QUR's potential, which is supported by substantial evidence, as a natural therapeutic agent in functional foods and dietary supplements that target fibrosis. However, further high-quality studies are essential to validate its safety, optimize formulation stability, and confirm clinical efficacy in order to ultimately expand its therapeutic applications.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-30"},"PeriodicalIF":0.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144577484","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}