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目的观察淫羊藿苷及睾酮对D-半乳糖所致亚急性衰老大鼠血清SOD活性、T、E2含量,睾丸组织P16蛋白表达与细胞凋亡的影响。方法随机将40只SD成年雄性大鼠分为正常对照组、模型组、淫羊藿组、睾酮组。检测各组大鼠血清SOD活性、T、E2含量,HE染色观察睾丸组织变化,SP法观察睾丸组织P16蛋白表达情况,TUNEL法检测睾丸生殖细胞凋亡情况。结果D-半乳糖致亚急性衰老大鼠血清SOD活性、T含量下降,与正常组比较差异显著(P<0．01,P<0．01);各组E2变化无统计学意义。睾丸组织出现退行性变化,睾丸生殖细胞P16阳性细胞百分率(PI)和凋亡指数增加,较正常组差异显著(P<0．01);淫羊藿组和睾酮组SOD活性增加,T水平升高,生殖细胞凋亡指数下降,较模型组差异显著,睾丸组织的退行性变化明显改善。淫羊藿组生殖细胞P16阳性细胞百分率较模型组差异显著(P<0．01),而睾酮组变化无显著意义。结论与睾酮相比,淫羊藿不仅可以提高亚急性衰老雄性大鼠血清SOD活性和雄激素水平,减少生殖细胞凋亡,改善睾丸组织的退行性变化,还可通过抑制生殖细胞衰老基因P16蛋白表达这一途径延缓性腺衰老。
Objective To observe the effects of icariin and testosterone on the activity of SOD, the content of T and E2, the expression of P16 protein and the apoptosis of testes in subacute aging rats induced by D-galactose. Methods 40 adult SD rats were randomly divided into normal control group, model group, Epimedium group and testosterone group. Detect the serum SOD activity, T, E2 content in each group, observe the changes of testis tissue by HE staining, observe the expression of P16 protein in testis tissue by SP method, and detect the germ cell apoptosis by TUNEL method. Results Serum SOD activity and T content of D-galactose induced subacute aging rats were significantly lower than those of normal rats (P <0.01, P <0.01). There was no significant difference in E2 between the two groups. (P <0.01). The activity of SOD in Epimedium and testosterone groups increased, and the level of T increased as the level of P16 positive cells increased (P <0.01) High, germ cell apoptosis index decreased significantly compared with the model group, testicular degeneration significantly improved. The percentage of P16 positive cells in the genital cells of Epimedium was significantly higher than that of the model group (P <0.01), but there was no significant change in the testosterone group. Conclusion Compared with testosterone, Epimedium can not only increase serum SOD activity and androgen levels in subacute aging male rats, reduce germ cell apoptosis, and improve degeneration of testicular tissue, but also inhibit the expression of P16 protein in germ cell senescence This pathway delays gonadal aging.