Activation of the p38/MAPK pathway regulates autophagy in response to the CYPOR-dependent oxidative stress induced by zearalenone in porcine intestinal epithelial cells

自噬 细胞生物学 MAPK/ERK通路 p38丝裂原活化蛋白激酶 程序性细胞死亡 氧化应激 细胞凋亡 活性氧 生物 化学 信号转导 生物化学
作者
Tongtong Shen,Yufan Miao,Chenchen Ding,Wentao Fan,Shuhui Liu,Yanan Lv,Xiaona Gao,Marthe De Boevre,Liping Yan,Sheila Okoth,Sarah De Saeger,Suquan Song
出处
期刊:Food and Chemical Toxicology [Elsevier]
卷期号:131: 110527-110527 被引量:38
标识
DOI:10.1016/j.fct.2019.05.035
摘要

Zearalenone (ZEA) can widely contaminate crops and agricultural products. The ingestion of ZEA-contaminated food or feed affects the integrity and functions of the intestines. In this study, we aimed to find the potential protective mechanism against ZEA ingestion. We found that ZEA induced cell death in IPEC-J2 cells. Meanwhile, the cytoprotective autophagy was activated in ZEA-treated cells. Further studies demonstrated that a p38/MAPK inhibitor down-regulated autophagy and increased cell death compared to those of the controls. Furthermore, ZEA could induce the accumulation of ROS, and eliminating ROS with NAC resulted in a decline in cell death, p38/MAPK phosphorylation, and the expression of LC3-II compared to those of ZEA-group. In addition, cytochrome P450 reductase (CYPOR) was significantly increased in ZEA-treated cells compared to that in the controls, and an inhibitor of CYPOR decreased ROS levels and mitigated cell death compared to those of the ZEA-group. More importantly, we found that blocking both p38/MAPK signalling and autophagy could enhance CYPOR expression and elevate ROS levels. Overall, our study indicated that the p38/MAPK pathway could activate protective autophagy in response to the CYPOR-dependent oxidative stress that was induced by ZEA in IPEC-J2 cells.
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