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.

中文翻译：

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硒代蛋氨酸通过 Bax-Caspase 途径减轻小鼠肠道缺血再灌注损伤。

已知硒代蛋氨酸 (SeMet) 可减轻缺血再灌注 (I/R) 损伤。然而，其在肠 I/R 损伤小鼠中的作用细节尚未完全阐明。本研究建立肠I/R损伤小鼠模型，ELISA检测谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、丙二醛（MDA）等氧化还原因子的含量。 )，在小鼠肠道组织中。此外，使用 qPCR 和蛋白质印迹检测了几种凋亡相关标志物，例如细胞色素 c (Cyt-c)、Bcl-2 和 Bax，而仅使用蛋白质印迹检测了 caspase-3。结果表明，SeMet 通过增加 GSH-Px、CAT 和 SOD 水平并降低 MDA 水平来减轻 I/R 损伤。我们的数据表明，SeMet 减少了 I/R 损伤并抑制了 Cyt-c、Bax 和 caspase-3 的表达。SeMet 还增加了小鼠肠道组织中 Bcl-2 的表达。此外，TUNEL 测定结果表明，SeMet 减轻了肠粘膜绒毛细胞的凋亡。研究结果还表明，I/R 可导致细胞凋亡水平增加，并且 SeMet 通过介导肠道 I/R 损伤小鼠模型中的 Bax/细胞色素 C/caspase-3 凋亡信号通路来减轻 I/R 诱导的细胞凋亡。因此，SeMet 抑制细胞凋亡并导致 Bcl-2 水平升高；下调 Bax、Cyt-c 和 caspase-3 的表达；并减轻小鼠肠道缺血损伤。I/R 损伤增加了细胞溶质 Bax、Cyt-c、与 Sham 组相比，I/R 组中 caspase-3 水平和 Caspase-3 水平显着降低，Bcl-2 表达水平显着降低。然而，所有标志物的水平在 SeMet 预处理后被逆转。