淫羊藿苷通过抑制 TLR4 介导的铁变态反应改善病毒性心肌炎

IF 16.4 1区 化学 Q1 CHEMISTRY, MULTIDISCIPLINARY Accounts of Chemical Research Pub Date : 2024-03-01 DOI:10.4103/apjtb.apjtb_588_23
Wei Luo, Yi Lu, Jun Deng, Peng Liu, Yan Huang, Wan-Xi Liu, Chun-Li Huang
{"title":"淫羊藿苷通过抑制 TLR4 介导的铁变态反应改善病毒性心肌炎","authors":"Wei Luo, Yi Lu, Jun Deng, Peng Liu, Yan Huang, Wan-Xi Liu, Chun-Li Huang","doi":"10.4103/apjtb.apjtb_588_23","DOIUrl":null,"url":null,"abstract":"\n \n To explore the mechanism by which icariin alleviates viral myocarditis.\n \n \n \n CVB3-induced cardiomyocytes were used as an in vitro model of viral myocarditis to assess the effects of icariin treatment on cell viability, inflammation, and apoptosis. Moreover, the effects of icariin on ferroptosis and TLR4 signaling were assessed. After AC16 cells were transfected with TLR4 overexpression plasmids, the role of TLR4 in mediating the regulatory effect of icariin in viral myocarditis was investigated.\n \n \n \n Icariin significantly elevated cell viability and reduced inflammatory factors TNF-α, IL-1β, IL-6, and IL-18. Flow cytometry revealed that icariin decreased apoptosis rate, and the protein expression of Bax and cleaved caspase 3 and 9 in CVB3-induced cardiomyocytes. Additionally, it suppressed ferroptosis including lipid peroxidation and ferrous ion, as well as the TLR4 signaling. However, TLR4 overexpression abrogated the modulatory effects of icariin.\n \n \n \n Icariin mitigates CVB3-induced myocardial injury by inhibiting TLR4-mediated ferroptosis. Further animal study is needed to verify its efficacy.\n","PeriodicalId":1,"journal":{"name":"Accounts of Chemical Research","volume":null,"pages":null},"PeriodicalIF":16.4000,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Icariin ameliorates viral myocarditis by inhibiting TLR4-mediated ferroptosis\",\"authors\":\"Wei Luo, Yi Lu, Jun Deng, Peng Liu, Yan Huang, Wan-Xi Liu, Chun-Li Huang\",\"doi\":\"10.4103/apjtb.apjtb_588_23\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"\\n \\n To explore the mechanism by which icariin alleviates viral myocarditis.\\n \\n \\n \\n CVB3-induced cardiomyocytes were used as an in vitro model of viral myocarditis to assess the effects of icariin treatment on cell viability, inflammation, and apoptosis. Moreover, the effects of icariin on ferroptosis and TLR4 signaling were assessed. After AC16 cells were transfected with TLR4 overexpression plasmids, the role of TLR4 in mediating the regulatory effect of icariin in viral myocarditis was investigated.\\n \\n \\n \\n Icariin significantly elevated cell viability and reduced inflammatory factors TNF-α, IL-1β, IL-6, and IL-18. Flow cytometry revealed that icariin decreased apoptosis rate, and the protein expression of Bax and cleaved caspase 3 and 9 in CVB3-induced cardiomyocytes. Additionally, it suppressed ferroptosis including lipid peroxidation and ferrous ion, as well as the TLR4 signaling. However, TLR4 overexpression abrogated the modulatory effects of icariin.\\n \\n \\n \\n Icariin mitigates CVB3-induced myocardial injury by inhibiting TLR4-mediated ferroptosis. Further animal study is needed to verify its efficacy.\\n\",\"PeriodicalId\":1,\"journal\":{\"name\":\"Accounts of Chemical Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":16.4000,\"publicationDate\":\"2024-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Accounts of Chemical Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.4103/apjtb.apjtb_588_23\",\"RegionNum\":1,\"RegionCategory\":\"化学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CHEMISTRY, MULTIDISCIPLINARY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Accounts of Chemical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.4103/apjtb.apjtb_588_23","RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}
引用次数: 0

摘要

探索冰片素缓解病毒性心肌炎的机制。 以 CVB3 诱导的心肌细胞作为病毒性心肌炎的体外模型,评估冰片苷处理对细胞活力、炎症和凋亡的影响。此外,还评估了冰片花素对铁变态反应和 TLR4 信号转导的影响。用 TLR4 过表达质粒转染 AC16 细胞后,研究了 TLR4 在病毒性心肌炎中介导冰片素调节作用的作用。 水淫羊藿苷明显提高了细胞活力,降低了炎症因子 TNF-α、IL-1β、IL-6 和 IL-18。流式细胞术显示,水淫羊藿苷降低了 CVB3 诱导的心肌细胞的凋亡率,以及 Bax 和裂解的 Caspase 3 和 9 的蛋白表达。此外,它还能抑制铁变态反应,包括脂质过氧化和亚铁离子,以及 TLR4 信号传导。然而,TLR4 的过表达会减弱淫羊藿苷的调节作用。 淫羊藿苷通过抑制 TLR4 介导的铁肽化来减轻 CVB3 诱导的心肌损伤。要验证其疗效,还需要进一步的动物实验。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Icariin ameliorates viral myocarditis by inhibiting TLR4-mediated ferroptosis
To explore the mechanism by which icariin alleviates viral myocarditis. CVB3-induced cardiomyocytes were used as an in vitro model of viral myocarditis to assess the effects of icariin treatment on cell viability, inflammation, and apoptosis. Moreover, the effects of icariin on ferroptosis and TLR4 signaling were assessed. After AC16 cells were transfected with TLR4 overexpression plasmids, the role of TLR4 in mediating the regulatory effect of icariin in viral myocarditis was investigated. Icariin significantly elevated cell viability and reduced inflammatory factors TNF-α, IL-1β, IL-6, and IL-18. Flow cytometry revealed that icariin decreased apoptosis rate, and the protein expression of Bax and cleaved caspase 3 and 9 in CVB3-induced cardiomyocytes. Additionally, it suppressed ferroptosis including lipid peroxidation and ferrous ion, as well as the TLR4 signaling. However, TLR4 overexpression abrogated the modulatory effects of icariin. Icariin mitigates CVB3-induced myocardial injury by inhibiting TLR4-mediated ferroptosis. Further animal study is needed to verify its efficacy.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Accounts of Chemical Research
Accounts of Chemical Research 化学-化学综合
CiteScore
31.40
自引率
1.10%
发文量
312
审稿时长
2 months
期刊介绍: Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.
期刊最新文献
Mentorship in academic musculoskeletal radiology: perspectives from a junior faculty member. Underlying synovial sarcoma undiagnosed for more than 20 years in a patient with regional pain: a case report. Sacrococcygeal chordoma with spontaneous regression due to a large hemorrhagic component. Associations of cumulative voriconazole dose, treatment duration, and alkaline phosphatase with voriconazole-induced periostitis. Can the presence of SLAP-5 lesions be predicted by using the critical shoulder angle in traumatic anterior shoulder instability?
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1