Selenomethionine Alleviates Intestinal Ischemia-Reperfusion Injury in Mice Through the Bax-Caspase Pathway.

Abstract

Selenomethionine (SeMet) is known to alleviate ischemia-reperfusion (I/R) injury. However, its details of action have not been thoroughly elucidated in mice with intestinal I/R injury. In this study, intestinal I/R injury mice models were established, and ELISAs were performed to determine the levels of redox factors, including glutathione peroxidase (GSH-Px), catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA), in mice intestinal tissues. Furthermore, several apoptosis-related markers, such as cytochrome c (Cyt-c), Bcl-2, and Bax, were detected using qPCR and Western blotting, while caspase-3 was detected using Western blotting alone. The results showed that SeMet alleviated I/R damage by increasing GSH-Px, CAT, and SOD levels and reducing MDA levels. Our data demonstrated that SeMet reduced I/R injury and inhibited the expression of Cyt-c, Bax, and caspase-3. SeMet also increased the expression of Bcl-2 in the intestinal tissues of mice. In addition, the TUNEL assay results showed that SeMet mitigated apoptosis in the villi cells of the intestinal mucosa. The findings also revealed that I/R could lead to increased apoptosis levels and that SeMet alleviated I/R-induced apoptosis by mediating the Bax/cytochrome C/caspase-3 apoptotic signaling pathways in the intestinal I/R injury mice models. Thus, SeMet inhibited apoptosis and resulted in an increase of Bcl-2 levels; downregulated the expression of Bax, Cyt-c, and caspase-3; and alleviated the intestinal ischemia injury in mice. The I/R injury increased the cytosolic Bax, Cyt-c, and caspase-3 levels and significantly decreased Bcl-2 expression levels in the I/R group, compared to the Sham group. However, the levels of all markers were reversed post-SeMet pre-treatment.