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

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Abstract
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.
Keywords
Zearalenone, Oxidative stress, Autophagy, CYPOR, p38/MAPK, FUMONISIN B1, DEOXYNIVALENOL, APOPTOSIS, TOXICITY, LIVER, BETA, CYTOCHROME-P450, MECHANISMS, EXPRESSION

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MLA
Shen, Tongtong, et al. “Activation of the P38/MAPK Pathway Regulates Autophagy in Response to the CYPOR-Dependent Oxidative Stress Induced by Zearalenone in Porcine Intestinal Epithelial Cells.” FOOD AND CHEMICAL TOXICOLOGY, vol. 131, 2019.
APA
Shen, T., Miao, Y., Ding, C., Fan, W., Liu, S., Lv, Y., … Song, S. (2019). Activation of the p38/MAPK pathway regulates autophagy in response to the CYPOR-dependent oxidative stress induced by zearalenone in porcine intestinal epithelial cells. FOOD AND CHEMICAL TOXICOLOGY, 131.
Chicago author-date
Shen, Tongtong, Yufan Miao, Chenchen Ding, Wentao Fan, Shuhui Liu, Yanan Lv, Xiaona Gao, et al. 2019. “Activation of the P38/MAPK Pathway Regulates Autophagy in Response to the CYPOR-Dependent Oxidative Stress Induced by Zearalenone in Porcine Intestinal Epithelial Cells.” FOOD AND CHEMICAL TOXICOLOGY 131.
Chicago author-date (all authors)
Shen, Tongtong, Yufan Miao, Chenchen Ding, Wentao Fan, Shuhui Liu, Yanan Lv, Xiaona Gao, Marthe De Boevre, Liping Yan, Sheila Okoth, Sarah De Saeger, and Suquan Song. 2019. “Activation of the P38/MAPK Pathway Regulates Autophagy in Response to the CYPOR-Dependent Oxidative Stress Induced by Zearalenone in Porcine Intestinal Epithelial Cells.” FOOD AND CHEMICAL TOXICOLOGY 131.
Vancouver
1.
Shen T, Miao Y, Ding C, Fan W, Liu S, Lv Y, et al. Activation of the p38/MAPK pathway regulates autophagy in response to the CYPOR-dependent oxidative stress induced by zearalenone in porcine intestinal epithelial cells. FOOD AND CHEMICAL TOXICOLOGY. 2019;131.
IEEE
[1]
T. Shen et al., “Activation of the p38/MAPK pathway regulates autophagy in response to the CYPOR-dependent oxidative stress induced by zearalenone in porcine intestinal epithelial cells,” FOOD AND CHEMICAL TOXICOLOGY, vol. 131, 2019.
@article{8662505,
  abstract     = {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.},
  articleno    = {110527},
  author       = {Shen, Tongtong and Miao, Yufan and Ding, Chenchen and Fan, Wentao and Liu, Shuhui and Lv, Yanan and Gao, Xiaona and De Boevre, Marthe and Yan, Liping and Okoth, Sheila and De Saeger, Sarah and Song, Suquan},
  issn         = {0278-6915},
  journal      = {FOOD AND CHEMICAL TOXICOLOGY},
  keywords     = {Zearalenone,Oxidative stress,Autophagy,CYPOR,p38/MAPK,FUMONISIN B1,DEOXYNIVALENOL,APOPTOSIS,TOXICITY,LIVER,BETA,CYTOCHROME-P450,MECHANISMS,EXPRESSION},
  language     = {eng},
  pages        = {10},
  title        = {Activation of the p38/MAPK pathway regulates autophagy in response to the CYPOR-dependent oxidative stress induced by zearalenone in porcine intestinal epithelial cells},
  url          = {http://dx.doi.org/10.1016/j.fct.2019.05.035},
  volume       = {131},
  year         = {2019},
}

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