PDF(Pubmed)
Abstract：
Deoxynivalenol (DON) is a prevalent contaminant in feed and food, posing a serious threat to the health of both humans and animals. The pig stands as an ideal subject for the study of DON due to its recognition as the most susceptible animal to DON. In this study, the IPEC-J2 cells were utilized as an in vitro model to explore the potential of SeMet in alleviating the intestinal toxicity and oxidative injury in intestinal epithelial cells when exposed to DON. Cells were treated either with or without 4.0 μM SeMet, in combination with or without a simultaneous treatment with 0.5 μg/mL DON, for a duration of 24 h. Then, cells or related samples were analyzed for cell proliferation, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) level, gene expressions, and protein expressions. The results showed that SeMet mitigated the cellular toxicity caused by DON, evidenced by elevated cell proliferation and the reduced LDH release of IPEC-J2 cells in the SeMet + DON group vs. the DON group. Moreover, the SeMet treatment markedly promoted antioxidant functions and decreased the oxidative injury in IPEC-J2 cell, which is indicated by the decreased ROS level and up-regulated mRNA levels of GPX1, TXNRD1, Nrf2, and GCLC in IPEC-J2 cells in the SeMet + DON group vs. the DON group. However, in both the absence and presence of exposure to DON, the SeMet treatment did not affect the protein expression of MAPK (JNK, Erk1/2, and P38) and phosphorylated MAPK (p-JNK, p-Erk1/2, and p-P38) in IPEC-J2 cells. Collectively, SeMet alleviated the DON-induced oxidative injury in porcine intestinal epithelial cells independent of the MAPK pathway regulation.
摘要：
脱氧雪腐镰刀菌烯醇(DON)是饲料和食品中普遍存在的污染物,对人类和动物的健康构成严重威胁。由于猪被认为是最容易感染DON的动物，因此猪是研究DON的理想对象。在这项研究中,利用IPEC-J2细胞作为体外模型,探讨SeMet在减轻暴露于DON时肠上皮细胞的肠毒性和氧化损伤方面的潜力.用或不用4.0μMSeMet处理细胞，联合或不联合0.5μg/mLDON同时治疗，持续24小时。然后，分析细胞或相关样品的细胞增殖，乳酸脱氢酶（LDH）释放，活性氧（ROS）水平，基因表达，和蛋白质表达。结果表明，SeMet减轻了DON引起的细胞毒性，SeMetDON组的细胞增殖升高和IPEC-J2细胞的LDH释放减少。DON组。此外，SeMet处理显著促进IPEC-J2细胞的抗氧化功能和减少氧化损伤,这表明在SeMet+DON组IPEC-J2细胞中ROS水平降低和GPX1、TXNRD1、Nrf2和GCLCmRNA水平上调。DON组。然而,在没有和存在接触DON的情况下，SeMet治疗不影响MAPK的蛋白表达(JNK，Erk1/2和P38）和磷酸化MAPK（p-JNK，p-Erk1/2和p-P38)在IPEC-J2细胞中。总的来说，SeMet减轻了DON诱导的猪肠上皮细胞氧化损伤，而与MAPK通路调节无关。
