17β-雌二醇对人精子功能非基因组调节效应的机制研究  

Mechanisms of Nongenomic Effect of 17β-Estradiol on Human Spermatozoa

作　　者：顾雪蓓[1] 张金虎[1] 岳利民[1] 王强 毛咏秋[2] 何亚萍[1] 

机构地区：[1]四川大学华西基础医学与法医学院生理学教研室,成都610041 [2]四川大学华西医院

出　　处：《四川大学学报（医学版）》2009年第5期861-864,共4页Journal of Sichuan University(Medical Sciences)

摘　　要：目的分析17β-雌二醇非基因组效应的可能机制。方法精子经各不同信号转导途径抑制剂处理后,再用10-6mol/L非透膜性偶联牛血清白蛋白雌二醇(E2-BSA)处理精子,采用流式细胞术检测精子胞内钙离子浓度的变化;采用Western blot检测信号蛋白的激活情况,探讨雌激素对人精子功能的非基因组调节效应的机制。结果用腺苷酸环化酶特异性抑制剂SQ22536、磷脂酶C(PLC)特异性抑制剂U73122和酪氨酸蛋白激酶特异性抑制剂Genistein处理精子后均明显抑制E2-BSA引起的精子胞内钙离子浓度的升高(P<0.05)。用Western blot方法检测到精子经10-6mol/LE2-BSA处理后,PLC和蛋白激酶C(PKC)均被激活,并且传统雌激素胞浆受体阻断剂tamoxifen不能抑制PLC的激活。结论17β-雌二醇可能通过腺苷酸环化酶、PLC或酪氨酸蛋白激酶信号转导途径实现对人精子功能调节的非基因组效应。Objective To study the mechanisms of nongenomic effect of 17β-estradiol on human spermatozoa. Methods The intracellular calcium（[Ca^2＋ ]i） in the spermatozoa was measured by flow cytometry after the spermatozoa was treated with the inhibitors of trans-membrane signaling transduction pathways and impermeable 17β-estradiol （E2-BSA）. Western blot was used to detect the activation of the signal proteins after the spermatozoa was treated with 1× 10^-6 mol/L E2-BSA and tamoxifen , an estrogen receptor inhibitor. Results Adenylyl cyclase （AC） inhibitor SQ22536, phospholipase C （PLC） inhibitor U73122 and protein tyrosine kinase （TPK） inhibitor Genistein all deterred the increase of [Ca^2＋ ]i caused by E2-BSA. E2-BSA also increased the PLC protein and PKC protein significantly. Tamoxifen, an antagonist of estrogen receptor, did not inhibit the activation of PLC caused by E2-BSA. Conclusion The E2-BSA has an effect on human spermatozoa in a nongenomie pathway, possibly through the transmembrane signal transduction in relation to AC, PLC and TPK.

关 键 词：人精子 17Β-雌二醇 非基因组效应 跨膜信号转导途径 

分 类 号：R96[医药卫生—药理学]