Chen W, Duan P, Tang S, Huang W T, Quan C, Qi S Q, Yang K D
MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2017 Feb 20;35(2):101-105. doi: 10.3760/cma.j.issn.1001-9391.2017.02.005.
To explore the effects of BPA on the expression of N-cadherin, Vimentin and FSHR in rat Sertoli cells. Primary Sertoli cells collected from prepuberty rats (18-21 d) were cultured for 48 h, and then they were treated with 0, 30, 50, 70 μmol/L BPA respectively for 24 h. The methods of MTT, real-time quantitative PCR and Western blotting were utilized to measure the cell ability of Sertoli cells, the mRNA and protein expression levels of N-cadherin, Vimentin and FSHR respectively. Compared with control, the cell abilities of Sertoli cells in 50 μmol/L BPA group and 70 μmol/L BPA group increased significantly (<0.05) . The cell abilities of Sertoli cells decreased with the increases of exposure doses of BPA. Compared with control, the expression of N-cadherin mRNA only increased in 30 μmol/L BPA group (<0.05) , the expression of Vimentin mRNA decreased significantly in all doses group of BPA (<0.05) , the expression of FSHR mRNA increased in all doses group of BPA (<0.05) . Compared with the control, the protein levels of N-cadherin increased significantly in 50 μmol/L BPA group (<0.05) , the protein levels of Vimentin decreased significantly in all doses group of BPA (<0.05) , the protein levels of FSHR decreased significantly in 50 μmol/L BPA group and 70 μmol/L BPA group (<0.05) . The mechanism of testicular toxicity from BPA might be the alterations of N-cadherin, Vimentin and FSHR by disturbing normal spermatogenesis.
探讨双酚A（BPA）对大鼠支持细胞中N-钙黏蛋白、波形蛋白和促卵泡激素受体（FSHR）表达的影响。收集青春期前大鼠（18 - 21日龄）的原代支持细胞，培养48小时，然后分别用0、30、50、70μmol/L的BPA处理24小时。采用MTT法、实时定量PCR法和蛋白质印迹法分别检测支持细胞的细胞活性、N-钙黏蛋白、波形蛋白和FSHR的mRNA及蛋白表达水平。与对照组相比，50μmol/L BPA组和70μmol/L BPA组支持细胞的细胞活性显著增加（<0.05）。支持细胞的细胞活性随BPA暴露剂量的增加而降低。与对照组相比，仅30μmol/L BPA组N-钙黏蛋白mRNA表达增加（<0.05），BPA各剂量组波形蛋白mRNA表达均显著降低（<0.05），BPA各剂量组FSHR mRNA表达均增加（<0.05）。与对照组相比，50μmol/L BPA组N-钙黏蛋白蛋白水平显著增加（<0.05），BPA各剂量组波形蛋白蛋白水平均显著降低（<0.05），50μmol/L BPA组和70μmol/L BPA组FSHR蛋白水平显著降低（<0.05）。BPA导致睾丸毒性的机制可能是通过干扰正常精子发生，改变N-钙黏蛋白、波形蛋白和FSHR。
