期刊
TOXINS
卷 10, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/toxins10010024
关键词
Zearalenone; cell cycle; cell apoptosis; ROS; ER stress; AMPK signaling; Sertoli cells; Zearalenone induced the cell cycle arrest and apoptosis through ROS-ER stress-AMPK pathway in mouse sertoli cells
资金
- National Key Research and Development Program of China [2016YFD0501208]
- National Natural Science Foundation of China [31372495, 31672620]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- ordinary university graduate student scientific research innovation projects in Jiangsu province [KYLX16_1406]
- excellent doctoral dissertation foundation of Yangzhou University
Zearalenone (ZEA) can perturb the differentiation of cells, reduce the generation of reproductive cells and induce a death of germ cells, but the molecular mechanism remains unclear. In order to investigate the potential mechanism of ZEA-induced cell cycle arrest and apoptosis, we studied the effects of ZEA on cell proliferation, cell-cycle distribution, cell-cycle-related proteins, cell death, cell apoptosis, ROS generation and the ATP/AMPK pathway in Sertoli cells. The role of ROS, ER stress and the ATP/AMPK pathway in ZEA-induced cell-cycle arrest and cell apoptosis was explored by using the antioxidant NAC, ER stress inhibitor 4-PBA and the AMPK inhibitor dorsomorphin, respectively. The results revealed that ZEA inhibited the cell proliferation, influenced the distribution of the cell cycle and induced cell apoptosis through the ATP/AMPK pathway. The ATP/AMPK pathway was regulated by ER stress that was induced by ROS generation after exposure to ZEA. Taking these together, this study provided evidence that ROS regulated the process of ZEA-induced cell cycle arrest and cell apoptosis through ER stress and the ATP/AMPK signal ways.
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