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目的研究全氟辛烷磺酰基化合物(perfluorooctane sulfonate,PFOS)对生精细胞凋亡的影响,并探讨其可能机制及G蛋白偶联受体30(G protein-coupled receptor 30,GPR30)在此过程中的作用。方法以GC-1小鼠精原细胞株为染毒模型,设置对照组和PFOS染毒组(50、100和200μmol/L)。运用MTT法检测GC-1细胞的存活率;Annexin VFITC/PI双染色法检测GC-1细胞凋亡;采用蛋白质印迹技术(Western blot)检测不同剂量PFOS及同时加入GPR30特异性阻断剂G15后对生精细胞凋亡相关蛋白表达的影响。结果 PFOS能够显著抑制GC-1细胞的增殖、促进GC-1细胞凋亡;PFOS染毒后,GC-1细胞中GPR30及凋亡相关蛋白Cleaved caspase-3、Bax表达显著升高;G15阻断GPR30的表达后,PFOS对Cleaved caspase-3表达水平的提升作用被部分逆转。结论 PFOS能显著促进生精细胞凋亡,其机制可能是通过上调GPR30的表达继而激活线粒体凋亡通路,并最终影响精子发生。
Objective To study the effect of perfluorooctane sulfonate (PFOS) on apoptosis of spermatogenic cells and to explore its possible mechanism and the mechanism of G protein-coupled receptor 30 (GPR30) In the role. Methods GC-1 mouse spermatogonial cell strain was used as a model to establish a control group and a PFOS-exposed group (50, 100 and 200 μmol / L). The survival rate of GC-1 cells was detected by MTT assay. The apoptosis of GC-1 cells was detected by Annexin VFITC / PI double staining method. Different doses of PFOS and G15-specific blockers were detected by Western blot On the apoptosis of spermatogenic cells related protein expression. Results PFOS could significantly inhibit the proliferation of GC-1 cells and promote the apoptosis of GC-1 cells. The expression of GPR30 and Cleaved caspase-3 and Bax in GC-1 cells was significantly increased after PFOS exposure. GPR30 expression, PFOS Cleaved caspase-3 expression levels were partially reversed. Conclusions PFOS can significantly promote the apoptosis of spermatogenic cells, and its mechanism may be through up-regulating the expression of GPR30 and then activating the mitochondrial apoptotic pathway and ultimately affecting spermatogenesis.