MAPK信号途径介导的17β-雌二醇快速激活人精子的研究

The Papid Effects of 17β-estrodiol Mediated through MAPK Pathways on Human Spermatozoon Activation

目的观察17β-雌二醇(E2)对人精子快速的非基因组激活效应,并探讨其相关的作用机制。方法雌激素受体拮抗剂Tamoxifen(0.05μmol/L)预处理20min后,分别用E2(1μmol/L)、雌二醇-牛血清白蛋白结合物(E2-BSA,5μmol/L)作用获能人精子15min,以三色法染色检测获能人精子顶体反应率,Western blotting检测丝裂原活化蛋白激酶(MAPK)蛋白的表达变化。结果 E2、E2-BSA均能提高人精子的顶体反应率和促进p42/p44磷酸化MAPK蛋白的表达,且两者的作用均可被Tamoxifen所阻断。结论人精子膜上可能存在膜雌激素受体(mER),雌激素与mER结合后可通过MAPK信号途径快速激活人精子。

Objective To study the rapid non-genie effect and mechanism of 17β- estradiol on human spermatozoon aetiation ,Metods Human spermatozoa were cultivated with E2 （1μmol/L） or E2 -BSA（5μmol/L） for 15 minutes after treated with tamoxifen（0. 05μmol/L）for 20 minutes. Aorosome reaction rates were scored by trichrome staining and MAPK activity was determined by Western blotting. Results E2 or E2. --BSA significantly increased the acresome reaction rates and MAPK activity （p42/p44）. The effects of E2 or E2 -BSA were able to be inhibited by tamoxlfen. Concluswns There may be some membrane estrogen receptors on the hum,m spermatozoa,which mediate the rapid activlitional effects of estrogen on human spermatozoa through MAPK pathways.