Piglet diarrhea and even death due to Clostridium perfringens (C. perfringens) type C infection have led to huge economic losses in the pig industry worldwide. C. perfringens beta2 (CPB2) toxin is the main virulence factor for this pathogen. MiR-140-5p can exacerbate toxin-induced toxicity of toxin to cells by promoting oxidative stress. However, the role of pig miR-140-5p (ssc-miR-140-5p) in piglet diarrhea caused by C. perfringens type C has not been studied. Here, we study investigated the function of ssc-miR-140-5p by generating an in vitro CPB2-induced injury model in intestinal porcine epithelial (IPEC-J2) cells. Our results revealed that transfection with an ssc-miR-140-5p inhibitor significantly increased the viability of CPB2-induced IPEC-J2 cells, decrease the release of lactate dehydrogenase (LDH) and reactive oxygen species (ROS), and inhibit inflammatory responses and apoptosis. In addition, vascular endothelial growth factor A (VEGFA) was identified as a direct target of ssc-miR-140-5p by luciferase reporter assay. Western blot analysis showed that inhibition of ssc-miR-140-5p could activate the ERK1/2 signaling pathway and inhibit the JNK signaling pathway. In summary, we showed that down-regulation of ssc-miR-140-5p ameliorated CPB2-induced inflammatory responses in IPEC-J2 cells via the ERK1/2 and JNK signaling pathways by targeting VEGFA.

由于C型产气荚膜梭状芽胞杆菌（C. perfringens）感染而导致的仔猪腹泻甚至死亡，已导致全世界养猪业的巨大经济损失。产气荚膜梭菌β2（CPB2）毒素是该病原体的主要毒力因子。MiR-140-5p可通过促进氧化应激而加剧毒素诱导的毒素对细胞的毒性。但是，尚未研究猪miR-140-5p（ssc-miR-140-5p）在由C型产气荚膜梭菌引起的仔猪腹泻中的作用。在这里，我们研究了通过体外产生ssc-miR-140-5p的功能CPB2诱导的肠猪上皮（IPEC-J2）细胞损伤模型。我们的结果表明，用ssc-miR-140-5p抑制剂转染可显着提高CPB2诱导的IPEC-J2细胞的活力，减少乳酸脱氢酶（LDH）和活性氧（ROS）的释放，并抑制炎症反应和细胞凋亡。此外，通过荧光素酶报告基因测定，血管内皮生长因子A（VEGFA）被确定为ssc-miR-140-5p的直接靶标。Western印迹分析表明，抑制ssc-miR-140-5p可以激活ERK1 / 2信号通路并抑制JNK信号通路。综上所述，我们发现在IPEC-J2细胞的SSC-的miR-140-5p改良后的CPB2引起的炎症反应是下调通过 通过靶向VEGFA来激活ERK1 / 2和JNK信号通路。