摘要
目的 研究人类精子囊性纤维化跨膜传导调节因子(CFTR)通过AMPK信号通道影响精子活力的机制.方法 使用CFTRinh-172 和毛喉素分别处理正常活力的精子和弱精症精子,检测精子活力、顶体酶活性、精子凋亡水平、细胞内ATP、ROS、线粒体膜电位(MMP),以及CFTR、AMPK、Bax和Bcl-2 的表达水平.结果 与各自对照组相比,CFTRinh-172 处理组的精子活力、顶体酶活性、ATP、MMP,以及CFTR、Bcl-2 的表达均降低,精子凋亡率、AMPK、Bax的表达升高;FSK处理组的精子活力、精子凋亡率、MMP、AMPK、Bax的表达均降低,顶体酶活性、ATP、CFTR、Bcl-2 的表达升高.结论 CFTR通过AMPK信号通路影响精子线粒体结构和功能,调控精子凋亡和活力.
Abstract
Objective To investigate the mechanism by which the cystic fibrosis transmembrane conductance regulator(CFTR)in human sperm influences sperm vitality through the AMPK signaling pathway.Methods Normal-vitality sperm and sperm with asthenozoospermia were treated with CFTRinh-172 and forskolin(FSK),respectively.Parameters including sperm vitality,acrosome enzyme activity,sperm apoptosis level,intracellular ATP,ROS,mitochondrial membrane potential(MMP),and the expression levels of CFTR,AMPK,Bax,and Bcl-2 were examined.Results CFTRinh-172 inhibited sperm vitality,acrosome enzyme activity,ATP,MMP,CFTR,and Bcl-2 expressions,also promoted sperm apoptosis rate,AMPK,and Bax expression.On the contrary,FSK treatment suppress sperm vitality,MMP,sperm apoptosis rate,AMPK,and Bax expressions,but elevated sperm acrosome enzyme activity,ATP,CFTR,and Bcl-2 levels.Conclusion CFTR influences sperm mitochondrial structure and function through the AMPK signaling pathway,and regulat sperm apoptosis and vitality.
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