BPA-induced apoptosis of rat Sertoli cells through Fas/FasL and JNKs/p38 MAPK pathways
BPA-induced apoptosis of rat Sertoli cells through Fas/FasL and JNKs/p38 MAPK pathways
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BPA 通过 Fas/FasL 和 JNKs/p38 MAPK 途径诱导大鼠支持细胞凋亡
DOI：
10.1016/j.reprotox.2014.10.013
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发表时间：
2014-12-01
影响因子：
3.3
通讯作者：
Yang, Kedi
中科院分区：
文献类型：
--
作者：
Qi, Suqin;Fu, Wenjuan;Yang, Kedi
双酚-A的影响进行了检查，从18日龄至22日龄的大鼠睾丸培养支持细胞。结果表明，暴露于BPA（0，30，50和70 μ M）以浓度依赖性方式降低细胞活力，并诱导细胞凋亡。在暴露于50和70 μ M BPA的细胞中观察到凋亡引起的细胞死亡。Fas、FasL和caspase-3的mRNA表达均升高，FasL和裂解型caspase-3的蛋白表达也升高。此外，JNKs/p38 MAPK的磷酸化水平也升高，激活后的JNKs/p38 MAPK可上调c-jun和CHOP等靶基因的表达。NF-κ B B转位到细胞核中表明BPA处理后NF-κ B活化。以上结果提示BPA通过激活JNKs/p38 MPAK和NF-κ B B转位诱导Sertoli细胞凋亡，Fas/FasL系统在凋亡的启动中起重要作用。(C)2014 Elsevier Inc. All rights reserved.
Bisphenol-A was examined for its effects on cultured Sertoli cells established from 18 to 22-day-old rat testes. Results indicated that exposure to BPA (0, 30, 50 and 70 mu M) decreased the cell viability in a concentration-dependent manner and induced cell apoptosis. Apoptosis-caused cell death was observed in cells exposed to 50 and 70 mu M BPA. The mRNA expressions of Fas, FasL and caspase-3 were all elevated, and the protein expressions of FasL and cleaved caspase-3 were also increased. In addition, levels of phosphorylation of JNKs/p38 MAPK were also increased and then activated JNKs/p38 MAPK up regulated target gene expressions, such as c-jun and CHOP. Translocation of NF-kappa B into nuclei indicated the activation of NF-kappa B after treatment with BPA. Taken together, observed results suggest that BPA induces apoptosis of Sertoli cells by the activation of JNKs/p38 MPAK and translocation of NF-kappa B, and Fas/FasL system plays a critical role in the initiation of apoptosis. (C) 2014 Elsevier Inc. All rights reserved.