中文摘要：脱氧雪腐镰刀菌烯醇（DON）是一种B型单端孢霉菌毒素，对人畜具有毒性作用。虽然在不同类型的细胞中研究了DON的细胞毒性，但很少涉及DON对小鼠子宫内膜基质细胞(ESCs)的作用的资料。因此，本研究探索了DON对小鼠ESCs的毒性作用及其可能的作用机制。结果表明在小鼠ESCs中，DON通过线粒体凋亡通路引起细胞凋亡，并通过p38 MAPK信号通路引起G2期阻滞。
外文摘要：Deoxynivalenol (DON) is a type B trichothecene mycotoxin which has toxic effects on humans and animals. Although DON has been studied in various cell types for its cytotoxicity, there is litter information about the effects of DON on mouse endometrial stromal cells (ESCs). Thus, in this study, we investigated the toxic effects of DON on mouse ESCs and its possible mechanisms. DON inhibited the cell viability in a dose- and time-dependent manner. TUNEL assay results showed that DON caused apoptosis and TUNEL-positive cells increased with increasing DON concentrations in mouse ESCs. Western blot showed that DON significantly increased the expression levels of apoptosis-related protein including Caspase-9, Caspase-3, poly (ADP-ribose) polymerase (PARP) and the ratio of Bax/Bcl-2. After DON treatment, the expression levels of cell cycle-related protein including p38/p-p38, Cdc25C/p-Cdc25C, Cdc2/p-Cdc2 and cyclinB1 were significantly decreased and immunoprecipitation analysis showed that cyclinB1-Cdc2 complex was significantly decreased. However, the combination of SB203580 (p38 specific inhibitor) and DON treatment significantly reversed the depression of Cdc25C/p-Cdc25C, Cdc2/p-Cdc2, cyclinB1 and cyclinB1-Cdc2 complex. Collectively, these data suggest that DON causes apoptosis via mitochondria apoptosis pathway and induces G2 arrest via p38 MAPK signaling pathway in mouse ESCs.
外文关键词：Deoxynivalenol；Mouse endometrial stromal cell；Cytotoxicity；Cell apoptosis；Cell cycle
作者：Dai, YJ；Xie, HQ；Xu, YX
作者单位：Nanjing Agr Univ
期刊名称：BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
期刊影响因子：2.371
出版年份：2017
出版刊次：1
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