Deoxynivalenol induced apoptosis and inflammation of IPEC-J2 cells by promoting ROS production
Deoxynivalenol induced apoptosis and inflammation of IPEC-J2 cells by promoting ROS production
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DOI：
10.1016/j.envpol.2019.05.026
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发表时间：
2019-08-01
影响因子：
8.9
通讯作者：
Li, Chunmei
中科院分区：
文献类型：
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作者：
Kang, Ruifen;Li, Ruonan;Li, Chunmei
脱氧雪腐镰刀菌烯醇(DON)广泛存在于各种食品和饲料中，对动物和人类都有细胞毒性作用。为探讨DON诱导猪小肠上皮细胞凋亡和炎症的可能机制，以猪小肠上皮细胞(IPEC-J2细胞)为研究对象，用不同浓度DON(0、0.2、0.5、1.0、2.0、4.0、6.0µg/mL)处理细胞。结果表明，DON以剂量依赖的方式诱导IPEC-J2细胞的细胞毒作用，表现为细胞活力下降。与对照组相比，DON处理组炎症和凋亡相关基因IL-1β、COX-2、IL-6、肿瘤坏死因子-α、caspase-3、caspase-8、caspase-9的表达增加，细胞抗氧化状态降低。蛋白免疫荧光显示IPEC-J2细胞中caspase-3、核因子-kB(NF-kappa B)和磷酸化的核因子-kappaB表达增加。DON可增加IPEC-J2细胞内ROS含量。常用抗氧化剂N-乙酰-L-半胱氨酸可阻断DON诱导的ROS生成，减轻DON诱导的细胞凋亡和炎症反应。这些结果提示DON诱导的IPEC-J2细胞损伤可能是由于ROS产生增加以及与细胞凋亡和炎症相关的基因和蛋白表达增加所致。(C)2019爱思唯尔有限公司。保留所有权利。
Deoxynivalenol (DON) frequently detected in a wide range of foods and feeds, inducing cytotoxicity to animals and humans. To investigate the underlying mechanism of DON-induced apoptosis and inflammation in porcine small intestinal epithelium, intestinal porcine epithelial cells (IPEC-J2 cells) were chosen as objects, and were treated by different concentrations (0 mu g/mL, 0.2 mu g/mL, 0.5 mu g/mL, 1.0 mu g/mL, 2.0 mu g/mL, 4.0 mu g/mL, 6.0 mu g/mL) of DON. The results showed that DON induced cytotoxicity of IPEC-J2 cells in a dose-dependent manner, which is demonstrated by decreasing cell viability. Compared with the control group, DON treatment increased the expressions of genes associated with inflammation and apoptosis, such as interleukin-1 beta (IL-1 beta), cyclooxgenase-2 (COX-2), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), caspase-3, caspase-8, caspase-9, and decreased the cell anti-oxidative status. Protein immunofluorescence showed increased expression of caspase-3, nuclear factor kB (NF-kappa B) and phosphorylated NF-kappa B in IPEC-J2 cells. DON increased the content of intracellular reactive oxygen species (ROS) of IPEC-J2 cells. N-Acetyl-L-cysteine (NAC), a commonly used antioxidant, blocked DON-induced ROS generation, alleviated the DON-induced apoptosis and inflammation. These results suggested that DON-induced impairment of IPEC-J2 cells is possibly due to increased ROS production, and expressions of genes and proteins associated with apoptosis and inflammation. (C) 2019 Elsevier Ltd. All rights reserved.