桂枝茯苓汤对精索静脉曲张大鼠生精细胞凋亡的作用机制OACHSSCD

Objective:To investigate the effects of Guizhi Fuling Decoction on spermatogenic cell apoptosis in a rat model of vari-cocele(VC)via regulation of the vascular endothelial growth factor/phosphatidylinositol 3-kinase/protein kinase B(VEGF/PI3K/AKT)signaling pathway.Methods:Sprague Dawley(SD)rats were randomly divided into five groups:normal control group(NC),VC model group(VC),VC+Guizhi Fuling Decoction low-dose group(GZFL-L),VC+Guizhi Fuling Decoction medium-dose group(GZFL-M),and VC+Guizhi Fuling Decoction high-dose group(GZFL-H).Testicular testosterone levels were measured using an automatic biochemical analyzer.Apoptosis of spermatogenic cells in rat testes was detected using a TUNEL assay.The expression levels of VEGF,AKT,phosphorylated AKT(p-AKT),p70 ribosomal S6 kinase(p70S6K),and phosphorylated p70S6K(p-p70S6K)were determined by immunofluorescence or immunohistochemistry.Results:Compared with the NC group,testicular testosterone levels in the VC group were significantly decreased.After treatment with different doses of Guizhi Fuling Decoction,testosterone lev-els in the GZFL-L,GZFL-M,and GZFL-H groups were increased compared with those in the VC group,with the most significant in-crease observed in the GZFL-H group(P＜0.05).Compared with the NC group,the number of apoptotic spermatogenic cells was significantly increased in the VC group(P＜0.05).Compared with the VC group,the number of apoptotic cells in the GZFL-L,GZ-FL-M,and GZFL-H groups was significantly reduced(P＜0.05).Compared with the NC group,VEGF protein expression was in-creased in the VC group,whereas VEGF expression was significantly decreased in the GZFL-L,GZFL-M,and GZFL-H groups(P＜0.05).In addition,compared with the NC group,the expression levels of p-AKT and p-p70S6K were increased in the VC group(both P＜0.05).Compared with the VC group,the expression levels of p-AKT and p-p70S6K were decreased in the GZFL-L,GZ-FL-M,and GZFL-H groups(P＜0.05).Conclusion:Guizhi Fuling Decoction may inhibit spermatogenic cell apoptosis in VC rats by blocking the VEGF/PI3K/AKT signaling pathway.