Selenomethionine Alleviates Intestinal Ischemia Reperfusion Injury by Inhibiting Mitochondrion-mediated Apoptosis in Mice 

Abstract

The mechanism of supplement selenomethionine (SeMet) mitigates ischemia reperfusion (I/R)- damage remains to be elucidated in the intestinal tissues of mice. In this study, a model of intestinal I/R injury was established. The levels of redox factors, such as the activities of glutathione peroxidase-1(Gpx1), catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) content, were detected using ELISA assays in the intestinal tissues of mice. Several apoptosis-related markers (cytochrome c (Cyt-c), Bcl-2, Bax, and caspase-3) were detected using qPCR and Western blot. The results showed that SeMet alleviated I/R damage by increasing the activities of Gpx1, CAT, SOD and reducing MDA content. Our data demonstrated that SeMet reduced I/R induced mitochondrial damage and inhibited the expression of Cyt-c. SeMet also increased the Bcl-2 /Bax ratio and reduced the expression of Bax and caspase-3 in the mice intestinal tissues. Thus our data reveals that I/R could lead to increased apoptosis, and SeMet alleviated I/ R-induced apoptosis via maintaining REDOX homeostasis and attenuating mitochondrial pathway in the mice intestinal tissues.