Deoxynivalenol hijacks the pathway of Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT-3) to drive caspase-3-mediated apoptosis in intestinal porcine epithelial cells
文献类型: 外文期刊
第一作者: Zhang, Zhiqi
作者: Zhang, Zhiqi;Fan, Kai;Meng, Jiajia;Nie, Dongxia;Zhao, Zhihui;Han, Zheng
作者机构:
关键词: Deoxynivalenol; IPEC-J2 cells; Apoptosis; STAT-3; Inflammation
期刊名称:SCIENCE OF THE TOTAL ENVIRONMENT ( 影响因子:9.8; 五年影响因子:9.6 )
ISSN: 0048-9697
年卷期: 2023 年 864 卷
页码:
收录情况: SCI
摘要: Deoxynivalenol (DON) can easily injure the intestinal tract, which represents the first barrier against food contami-nants. The intestinal toxicity induced by DON was mainly focused on mitogen-activated protein kinase (MAPK) acti-vation, however, the underlying mechanisms by which DON triggers apoptosis by other pathways remain poorly understood. In this study, the Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT-3) path-way was proposed to regulate the intrinsic apoptosis induced by DON and thoroughly investigated in intestinal porcine epithelial cells (IPEC-J2). First, DON was found to be able to efficiently inhibit cell viability and increase the release of lactate dehydrogenase. It could also enhance the activity of the cleaved caspase-3 in a time-dependent manner, accom-panied by a loss of mitochondrial membrane potential and an up-regulation of the apoptosis rate. Then, the expression of genes associated with inflammation and apoptosis were investigated. DON increased the expression of IL-6, IL-1 beta, TNF-alpha, SOCS3 and Bax, but decreased the expression of Bcl-2 and Bcl-xL. Moreover, we discovered that DON robustly inhibited STAT-3 activity together with the down-regulation of JAK2, Bcl-2 and Bcl-xL, paralleling the increase in p38 phosphorylation. Furthermore, a pharmacological activation of JAK2/STAT-3 alleviated DON induced-apoptosis. Con-current with the apoptotic pathway, during the initial exposure to DON (first 4 h), a survival pathway involving phos-phorylated Erk1/2, Akt, and FoxO1 was also observed. Thus, apoptosis induced by DON was Janus faced: although the survival pathway was activated, the DON-induced apoptotic JAK2/STAT-3/caspase-3 pathway dominated, leading to an imbalance in cell homeostasis. This study provides a novel avenue to comprehensively reveal the pathological mechanisms of DON-induced intestinal disorders, which is promising for future applications to other contaminants in food and feed.
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