Syringin alleviates ROS-induced acute lung injury by activating SIRT1/STAT6 signaling pathway to inhibit ferroptosis

IF 2.5 4区 生物学 Q1 ANATOMY & MORPHOLOGY Tissue & cell Pub Date : 2025-04-01 Epub Date: 2024-12-24 DOI:10.1016/j.tice.2024.102698
Xuemei Cai , Yanan Wu , Fuxia Liu , Jinping He , Yanhua Bi
{"title":"Syringin alleviates ROS-induced acute lung injury by activating SIRT1/STAT6 signaling pathway to inhibit ferroptosis","authors":"Xuemei Cai ,&nbsp;Yanan Wu ,&nbsp;Fuxia Liu ,&nbsp;Jinping He ,&nbsp;Yanhua Bi","doi":"10.1016/j.tice.2024.102698","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><div>Acute lung injury (ALI) is the critical respiratory condition. Syringin with anti-inflammatory and anti-oxidant properties can exhibit the lung protective effects. SIRT1 and STAT6 can exert protective roles against lung injury by inhibiting ferroptosis.</div></div><div><h3>Methods</h3><div>In the current study, A549 lung epithelial cells were treated with 200 μM H<sub>2</sub>O<sub>2</sub> for 2 h to establish an <em>in vitro</em> ALI model. Then, H<sub>2</sub>O<sub>2</sub>-stimulated A549 cells were treated with syringin to identify the biological role of syringin in ROS-induced ALI. Moreover, H<sub>2</sub>O<sub>2</sub>-stimulated A549 cells were further treated with SIRT1 inhibitor EX527 or ferroptosis activator erastin to elucidate whether syringin could exert protective effects against ROS-induced ALI depending on SIRT1/STAT6 signaling-mediated ferroptosis inhibition.</div></div><div><h3>Results</h3><div>It was verified that syringin treatment improved the impaired viability and mitigated inflammatory response and oxidative stress of H<sub>2</sub>O<sub>2</sub>-stimulated A549 lung epithelial cells by activating SIRT1/STAT6 signaling pathway. Syringin treatment inhibited the ferroptosis of H<sub>2</sub>O<sub>2</sub>-stimulated A549 lung epithelial cells by activating SIRT1/STAT6 signaling pathway. Treatment with SIRT1 inhibitor EX527 or ferroptosis activator erastin both reversed the alleviating effect of syringin on H<sub>2</sub>O<sub>2</sub>-induced A549 lung epithelial cell injury.</div></div><div><h3>Conclusion</h3><div>To sum up, syringin treatment alleviates H<sub>2</sub>O<sub>2</sub>-induced lung epithelial cell injury by activating SIRT1/STAT6 signaling pathway to inhibit ferroptosis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102698"},"PeriodicalIF":2.5000,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tissue & cell","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0040816624003999","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/24 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"ANATOMY & MORPHOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction

Acute lung injury (ALI) is the critical respiratory condition. Syringin with anti-inflammatory and anti-oxidant properties can exhibit the lung protective effects. SIRT1 and STAT6 can exert protective roles against lung injury by inhibiting ferroptosis.

Methods

In the current study, A549 lung epithelial cells were treated with 200 μM H2O2 for 2 h to establish an in vitro ALI model. Then, H2O2-stimulated A549 cells were treated with syringin to identify the biological role of syringin in ROS-induced ALI. Moreover, H2O2-stimulated A549 cells were further treated with SIRT1 inhibitor EX527 or ferroptosis activator erastin to elucidate whether syringin could exert protective effects against ROS-induced ALI depending on SIRT1/STAT6 signaling-mediated ferroptosis inhibition.

Results

It was verified that syringin treatment improved the impaired viability and mitigated inflammatory response and oxidative stress of H2O2-stimulated A549 lung epithelial cells by activating SIRT1/STAT6 signaling pathway. Syringin treatment inhibited the ferroptosis of H2O2-stimulated A549 lung epithelial cells by activating SIRT1/STAT6 signaling pathway. Treatment with SIRT1 inhibitor EX527 or ferroptosis activator erastin both reversed the alleviating effect of syringin on H2O2-induced A549 lung epithelial cell injury.

Conclusion

To sum up, syringin treatment alleviates H2O2-induced lung epithelial cell injury by activating SIRT1/STAT6 signaling pathway to inhibit ferroptosis.
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
紫丁香苷通过激活 SIRT1/STAT6 信号通路来抑制铁凋亡,从而减轻 ROS 诱导的急性肺损伤。
急性肺损伤(Acute lung injury, ALI)是一种危重的呼吸系统疾病。紫丁香素具有抗炎、抗氧化作用,对肺有保护作用。SIRT1和STAT6可通过抑制铁下垂对肺损伤发挥保护作用。方法:本研究采用200 μM H2O2处理A549肺上皮细胞2 h建立体外ALI模型。然后,用紫丁香素处理h2o2刺激的A549细胞,以确定紫丁香素在ros诱导的ALI中的生物学作用。此外,我们进一步用SIRT1抑制剂EX527或铁衰亡激活剂erastin处理h2o2刺激的A549细胞,以阐明紫丁香素是否通过SIRT1/STAT6信号介导的铁衰亡抑制对ros诱导的ALI发挥保护作用。结果:证实紫丁香素通过激活SIRT1/STAT6信号通路,改善h2o2刺激下A549肺上皮细胞受损的生存能力,减轻炎症反应和氧化应激。紫丁香素通过激活SIRT1/STAT6信号通路抑制h2o2刺激的A549肺上皮细胞铁下垂。SIRT1抑制剂EX527或铁下垂激活剂erastin治疗均逆转了紫丁香苷对h2o2诱导的A549肺上皮细胞损伤的缓解作用。结论:综上所述,紫丁香素通过激活SIRT1/STAT6信号通路抑制铁上吊,减轻h2o2诱导的肺上皮细胞损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Tissue & cell
Tissue & cell 医学-解剖学与形态学
CiteScore
3.90
自引率
0.00%
发文量
234
期刊介绍: Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed. Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.
期刊最新文献
Role of ferroptosis and autophagy in pulmonary diseases Oxidative stress and mitochondrial dysfunction contribute to pulmonary impairment in a murine model of type 2 diabetes mellitus Biochemical markers of muscle damage and recovery: Insights from exercise physiology and molecular biology Sperm morphology and ultrastructure in four species of ground beetles (Insects‐Carabidae) Engineering the cartilage niche: Mimicking the microenvironment for functional outcomes
×
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:604180095
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