Mechanism Analysis of UCP2 During the Oxidative Stress Injury of Intestinal Porcine Epithelial Cell Line-J2
文献类型： 外文期刊
作者： Su, Weide 1 ; Xu, Chuanhui 1 ; Jiang, Hongping 1 ; Song, Wenjing 1 ; Xiong, Pingwen 1 ; Chen, Jiang 1 ; Ai, Gaoxiang 1 ; Song, Qiongli 1 ; Zou, Zhiheng 1 ; Wei, Qipeng 1 ; Chen, Xiaolian 1 ;
作者机构： 1.Jiangxi Acad Agr Sci, Inst Anim Husb & Vet Med, Nanchang 330200, Peoples R China
2.Jiangxi Prov Key Lab Anim Green & Hlth Breeding, Nanchang 330200, Peoples R China
关键词： UCP2; oxidative stress; porcine intestinal epithelial cells; genipin; apoptosis
期刊名称：ANIMALS （ 影响因子：2.7； 五年影响因子：3.2 ）
ISSN： 2076-2615
年卷期： 2025 年 15 卷 11 期
页码：
收录情况： SCI
摘要： Oxidative stress poses a significant challenge in livestock production, impairing intestinal function, nutrient absorption, and overall animal performance. Uncoupling protein 2 (UCP2) is a mitochondrial regulator known for its protective effects against oxidative damage, but its specific function in porcine intestinal epithelial cells and its regulation by genipin-a natural UCP2 inhibitor with potential therapeutic properties-remains unclear. In this study, we cloned and overexpressed the porcine UCP2 gene in intestinal porcine epithelial cells (IPEC-J2), generating a stable UCP2-overexpressing cell line (IPEC-J2-UCP2). Under hydrogen peroxide-induced oxidative stress, UCP2 overexpression significantly improved cell viability, reduced reactive oxygen species (ROS) levels, and enhanced antioxidant enzyme activities (SOD, GPx, and CAT). Additionally, UCP2 upregulated the anti-apoptotic gene Bcl-2 and downregulated pro-apoptotic genes (Fas, Caspase-3, and Bax), indicating a protective role against oxidative stress-induced apoptosis. We also investigated the regulatory effects of genipin on UCP2. Under non-stress conditions, genipin mildly promoted anti-apoptotic gene expression. However, under oxidative stress, genipin strongly inhibited UCP2 expression, exacerbated ROS accumulation, reduced cell viability, and increased expression of pro-apoptotic markers, particularly Caspase-3 and Bax. These findings reveal that UCP2 plays a critical role in protecting porcine intestinal epithelial cells from oxidative injury and that genipin exerts context-dependent effects on cell fate by modulating UCP2. This study provides a mechanistic basis for targeting UCP2 to manage oxidative stress and improve intestinal health and performance in pigs.
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