Selenium (Se) plays a crucial role in intestinal health. However, the specific mechanism by which deficiency of Se causes intestinal damage remains unclear. This study was to explore whether Se deficiency can cause ER stress and induce apoptosis in swine small intestine. We established the Se deficiency swine model in vivo and the intestinal epithelial (IPEC-J2) cell Se deficiency model in vitro. The results of morphological observation showed that Se deficiency caused structural damage in intestinal villi and the decrease of goblet cell structure. The apoptotic characteristics such as nucleolar condensation, mitochondrial swelling, and apoptotic bodies were observed in the IPEC-J2 cells. The results of acridine orange/ethidium bromide and mitochondrial membrane potential fluorescence staining in vitro showed that there were more apoptotic cells in the Se-deficiency group than that in the control group. The protein and/or mRNA expression levels of Bax, Bcl-2, caspase 3, caspase 8, caspase 9, cytc, PERK, ATF6, IRE, XBP1, CHOP, GRP78, which are related to ER stress-apoptosis pathway, were significantly increased in the Se-deficient group which compared with the control group in vivo and in vitro were consistent. These results indicated that Se deficiency induced ER stress and increased the apoptosis in swine small intestine and IPEC-J2 cells and then caused the damage in swine small intestinal tissue. Besides, the results of gene expressions in our experiment proved that ER stress induced by Se deficiency promoted apoptosis. These results filled the blank in the mechanism of Se deficiency-induced intestinal injury in swine.

中文翻译：

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缺硒通过猪小肠内质网应激引起细胞凋亡

硒 (Se) 在肠道健康中起着至关重要的作用。然而，硒缺乏导致肠道损伤的具体机制仍不清楚。本研究旨在探讨硒缺乏是否会引起内质网应激并诱导猪小肠细胞凋亡。我们建立了体内缺硒猪模型和体外肠上皮（IPEC-J2）细胞缺硒模型。形态学观察结果表明，硒缺乏引起肠绒毛结构损伤，杯状细胞结构减少。在IPEC-J2细胞中观察到核仁浓缩、线粒体肿胀和凋亡小体等凋亡特征。体外吖啶橙/溴化乙锭和线粒体膜电位荧光染色结果显示，缺硒组凋亡细胞多于对照组。与ER应激-凋亡通路相关的Bax、Bcl-2、caspase 3、caspase 8、caspase 9、cytc、PERK、ATF6、IRE、XBP1、CHOP、GRP78的蛋白和/或mRNA表达水平显着升高。与对照组相比，硒缺乏组在体内和体外的增加是一致的。这些结果表明，硒缺乏诱导内质网应激，增加了猪小肠和IPEC-J2细胞的凋亡，进而引起猪小肠组织的损伤。此外，我们实验中基因表达的结果证明，硒缺乏诱导的内质网应激促进了细胞凋亡。