ArticleAnimals : an open access journal from MDPI2025
Mechanism Analysis of UCP2 During the Oxidative Stress Injury of Intestinal Porcine Epithelial Cell Line-J2.
Article in Animals : an open access journal from MDPI, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Stanniocalcin-1 Overexpression Protects Porcine Intestinal Epithelial Cells Against TBHP-Induced Oxidative Stress by Preserving Mitochondrial Homeostasis.Animals : an open access journal from MDPI · 2026Article
- Hindgut-targeted delivery alpha-ketoglutarate pellets improves broiler intestinal redox and growth performance by activating uncoupling protein 2.Poultry science · 2026Article
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11 authors.
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Abstract
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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