{"title":"Desflurane attenuates renal ischemia-reperfusion injury by modulating ITGB1/CD9 and reducing oxidative stress in tubular epithelial cells","authors":"Qiaoling Wu, Dongbo Zhang, Siqi Dai, Feifei Liu, Wei Zhang, Tu Shen","doi":"10.1016/j.redox.2025.103490","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><div>Renal ischemia-reperfusion (I/R) injury triggers significant oxidative stress and inflammation, leading to tubular epithelial cell (TEC) damage. This study investigates the protective role of Desflurane (DFE) in renal I/R by modulating the ITGB1/CD9 signaling pathway and mitigating oxidative damage.</div></div><div><h3>Methods</h3><div>Single-cell RNA sequencing (scRNA-seq) and transcriptome analysis identified ITGB1 as a key regulatory gene in TECs during renal I/R. The effects of DFE on ITGB1/CD9 expression were evaluated through <em>in vitro</em> experiments using RT-qPCR, Western blot, and TUNEL assays. A mouse model of renal I/R was employed to assess renal function and oxidative stress markers under DFE treatment.</div></div><div><h3>Results</h3><div>DFE reduced ITGB1 and CD9 expression, resulting in decreased TEC apoptosis and enhanced proliferation. <em>In vivo</em>, DFE-treated mice exhibited improved renal function, with significantly lower serum creatinine and blood urea nitrogen (BUN) levels. Additionally, DFE reduced oxidative stress, as indicated by decreased malondialdehyde (MDA) and myeloperoxidase (MPO) activity, alongside increased superoxide dismutase (SOD) activity.</div></div><div><h3>Conclusion</h3><div>DFE confers renal protection against I/R by modulating the ITGB1/CD9 axis and reducing oxidative stress, offering a promising therapeutic strategy for mitigating kidney damage.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"80 ","pages":"Article 103490"},"PeriodicalIF":10.7000,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Redox Biology","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2213231725000035","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective
Renal ischemia-reperfusion (I/R) injury triggers significant oxidative stress and inflammation, leading to tubular epithelial cell (TEC) damage. This study investigates the protective role of Desflurane (DFE) in renal I/R by modulating the ITGB1/CD9 signaling pathway and mitigating oxidative damage.
Methods
Single-cell RNA sequencing (scRNA-seq) and transcriptome analysis identified ITGB1 as a key regulatory gene in TECs during renal I/R. The effects of DFE on ITGB1/CD9 expression were evaluated through in vitro experiments using RT-qPCR, Western blot, and TUNEL assays. A mouse model of renal I/R was employed to assess renal function and oxidative stress markers under DFE treatment.
Results
DFE reduced ITGB1 and CD9 expression, resulting in decreased TEC apoptosis and enhanced proliferation. In vivo, DFE-treated mice exhibited improved renal function, with significantly lower serum creatinine and blood urea nitrogen (BUN) levels. Additionally, DFE reduced oxidative stress, as indicated by decreased malondialdehyde (MDA) and myeloperoxidase (MPO) activity, alongside increased superoxide dismutase (SOD) activity.
Conclusion
DFE confers renal protection against I/R by modulating the ITGB1/CD9 axis and reducing oxidative stress, offering a promising therapeutic strategy for mitigating kidney damage.
期刊介绍:
Redox Biology is the official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe. It is also affiliated with the International Society for Free Radical Research (SFRRI). This journal serves as a platform for publishing pioneering research, innovative methods, and comprehensive review articles in the field of redox biology, encompassing both health and disease.
Redox Biology welcomes various forms of contributions, including research articles (short or full communications), methods, mini-reviews, and commentaries. Through its diverse range of published content, Redox Biology aims to foster advancements and insights in the understanding of redox biology and its implications.