{"title":"Selenium inhibits ferroptosis in ulcerative colitis through the induction of Nrf2/Gpx4","authors":"","doi":"10.1016/j.clinre.2024.102467","DOIUrl":null,"url":null,"abstract":"<div><h3>Background and aim</h3><div>Selenium, an essential micronutrient for human and has been reported to have a protective effect in ulcerative colitis (UC). However, the role of selenium in UC is unclear. Our aim was to investigate the mechanism of action of selenium in UC.</div></div><div><h3>Methods</h3><div>Serum selenium levels were measured in UC patients and healthy controls. In addition, the effect of sodium selenite supplementation on experimental colitis in mice treated with dextran sulfate sodium (DSS) was investigated. The effect of sodium selenite on IECs ferroptosis was evaluated by observing the cell mortality, intracellular ferrous content, lipid reactive oxygen species and mitochondrial membrane damage in DSS-treated Caco2 cells. In addition, glutathione peroxidase 4 (Gpx4) and nuclear factor erythroid 2-like 2 (Nrf2) were detected in Caco2 cells and mouse intestines to explore their mechanisms.</div></div><div><h3>Results</h3><div>The serum selenium content of UC patients was lower than that of healthy subjects. In addition, serum selenium levels were negatively correlated with disease activity. The in vivo results showed that selenium treatment could improve colitis induced by DSS and inhibit IECs ferroptosis. The in vitro results further showed that selenium inhibited the ferroptosis of Caco-2 cells induced by DSS. Nrf2/Gpx4 was up-regulated after selenium supplementation in vivo and in vitro.</div></div><div><h3>Conclusions</h3><div>Serum selenium level is associated with IECs ferroptosis in UC patients. Selenium can relieve DSS-induced colitis and inhibit IECs ferroptosis by up-regulating the expression of Nrf2/Gpx4.</div></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":null,"pages":null},"PeriodicalIF":2.6000,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinics and research in hepatology and gastroenterology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2210740124001888","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background and aim
Selenium, an essential micronutrient for human and has been reported to have a protective effect in ulcerative colitis (UC). However, the role of selenium in UC is unclear. Our aim was to investigate the mechanism of action of selenium in UC.
Methods
Serum selenium levels were measured in UC patients and healthy controls. In addition, the effect of sodium selenite supplementation on experimental colitis in mice treated with dextran sulfate sodium (DSS) was investigated. The effect of sodium selenite on IECs ferroptosis was evaluated by observing the cell mortality, intracellular ferrous content, lipid reactive oxygen species and mitochondrial membrane damage in DSS-treated Caco2 cells. In addition, glutathione peroxidase 4 (Gpx4) and nuclear factor erythroid 2-like 2 (Nrf2) were detected in Caco2 cells and mouse intestines to explore their mechanisms.
Results
The serum selenium content of UC patients was lower than that of healthy subjects. In addition, serum selenium levels were negatively correlated with disease activity. The in vivo results showed that selenium treatment could improve colitis induced by DSS and inhibit IECs ferroptosis. The in vitro results further showed that selenium inhibited the ferroptosis of Caco-2 cells induced by DSS. Nrf2/Gpx4 was up-regulated after selenium supplementation in vivo and in vitro.
Conclusions
Serum selenium level is associated with IECs ferroptosis in UC patients. Selenium can relieve DSS-induced colitis and inhibit IECs ferroptosis by up-regulating the expression of Nrf2/Gpx4.
期刊介绍：
Clinics and Research in Hepatology and Gastroenterology publishes high-quality original research papers in the field of hepatology and gastroenterology. The editors put the accent on rapid communication of new research and clinical developments and so called "hot topic" issues. Following a clear Editorial line, besides original articles and case reports, each issue features editorials, commentaries and reviews. The journal encourages research and discussion between all those involved in the specialty on an international level. All articles are peer reviewed by international experts, the articles in press are online and indexed in the international databases (Current Contents, Pubmed, Scopus, Science Direct).
Clinics and Research in Hepatology and Gastroenterology is a subscription journal (with optional open access), which allows you to publish your research without any cost to you (unless you proactively chose the open access option). Your article will be available to all researchers around the globe whose institution has a subscription to the journal.
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
