Deoxynivalenol (DON) is considered to be the most harmful mycotoxin that affects the intestinal health of animals and humans. Phenethyl isothiocyanate (PEITC) in feedstuff is an anti-nutritional factor and impairs nutrient digestion and absorption in the animal intestinal. In the current study, we aimed to explore the effects of PEITC on DON-induced apoptosis, intestinal tight junction disorder, and its potential molecular mechanism in the porcine jejunum epithelial cell line (IPEC-J2). Our results indicated that PEITC treatment markedly alleviated DON-induced cytotoxicity, decreasing the apoptotic cell percentage and pro-apoptotic mRNA/protein levels, and increasing zonula occludens-1 (ZO-1), occludin and claudin-1 mRNA/protein expression. Meanwhile, PEITC treatment ameliorated DON-induced an increase of the inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) mRNA levels and intracellular reactive oxygen species (ROS) level, and a decrease of glutathione peroxidase 1 (GPx1), superoxide dismutase 2 (SOD2), catalase (CAT) and heme oxygenase 1 (HO-1) mRNA levels. Additionally, PEITC treatment significantly down-regulated autophagy-related protein 5 (ATG5), beclin-1 and microtubule-associated protein 1 light chain 3B (LC3-Ⅱ) mRNA/protein levels, decreased the number of green fluorescent protein-microtubule-associated protein 1 light-chain 3 (GFP-LC3) puncta and phosphatidylinositol 3 kinase (PI3K) protein expression, and up-regulated phospho-protein kinase B (p-Akt) and phospho-mammalian target of rapamycin (p-mTOR) protein expression against DON. However, the activation of autophagy by rapamycin, an autophagy agonist, abolished the protective effects of PEITC against DON-induced cytotoxicity, apoptosis and intestinal tight junction disorder. Collectively, PEITC could confer protection against DON-induced porcine intestinal epithelial cell injury by suppressing ROS-mediated autophagy.

脱氧雪腐镰刀菌烯醇 (DON) 被认为是影响动物和人类肠道健康的最有害的霉菌毒素。饲料中的异硫氰酸苯乙酯（PEITC）是一种抗营养因子，会损害动物肠道中营养物质的消化和吸收。在本研究中，我们旨在探讨PEITC对猪空肠上皮细胞系（IPEC-J2）DON诱导的细胞凋亡、肠紧密连接紊乱的影响及其潜在分子机制。我们的结果表明，PEITC 治疗显着减轻了 DON 诱导的细胞毒性，降低了凋亡细胞百分比和促凋亡 mRNA/蛋白水平，并增加了 zonula occlusionns-1 (ZO-1)、occludin 和 claudin-1 mRNA/蛋白表达。同时，PEITC 治疗改善了 DON 诱导的诱导型一氧化氮合酶 ( iNOS ) 和环氧合酶 2 ( COX-2 ) mRNA 水平和细胞内活性氧 (ROS) 水平的增加，以及谷胱甘肽过氧化物酶 1 ( GPx1 )的减少，超氧化物歧化酶 2 ( SOD2 )、过氧化氢酶 ( CAT ) 和血红素加氧酶 1 ( HO-1 ) mRNA 水平。此外，PEITC处理显着下调自噬相关蛋白5（ATG5）、beclin-1和微管相关蛋白1轻链3B（LC3-Ⅱ）mRNA/蛋白水平，减少微管相关绿色荧光蛋白的数量蛋白 1 轻链 3 (GFP-LC3) 点和磷脂酰肌醇 3 激酶 (PI3K) 蛋白表达，上调磷酸蛋白激酶 B (p-Akt) 和雷帕霉素磷酸化哺乳动物靶标 (p-mTOR) 蛋白表达反对唐。然而，自噬激动剂雷帕霉素对自噬的激活消除了 PEITC 对 DON 诱导的细胞毒性、细胞凋亡和肠道紧密连接紊乱的保护作用。总的来说，PEITC 可以通过抑制 ROS 介导的自噬来防止 DON 诱导的猪肠上皮细胞损伤。