外源性雄激素通过诱导自噬促大鼠睾丸萎缩的发生
首发时间:2018-09-30
摘要:目的探讨外源性雄激素对大鼠睾丸萎缩的影响及其可能机制。方法 48只SD雄性大鼠随机分成6组,每组8只:对照组(control)、雄激素(丙酸睾丸酮,TP)组、雄激素+氯喹组(TP+CQ)、雄激素+甘草甜素组(TP+Gly)、氯喹(CQ,自噬抑制剂)组、甘草甜素(Gly,HMGB1抑制剂)组。各组大鼠分别处理21d后,测量大鼠体重、睾丸湿重、睾丸指数;采用HE染色法观察大鼠睾丸组织病理学改变;Western-Blotting法检测大鼠睾丸组织Beclin-1、LC3B-II、p62、HMGB1蛋白的表达情况。结果给予大鼠TP干预21d后,大鼠睾丸湿重、睾丸指数均降低(P<0.01);睾丸生精小管发生萎缩,各级生精细胞排列紊乱、层数减少,未见成熟的精子;睾丸组织Beclin-1、LC3B-II和HMGB1蛋白表达均上调(P<0.05),p62蛋白表达无明显变化(P>0.05)。联合给予TP和CQ后,大鼠睾丸指数增加(P<0.05);生精小管和各级生精细胞损伤明显改善,可见到成熟的精子;睾丸组织Beclin-1、LC3B-II和HMGB1蛋白表达水平均下调(P<0.05),p62蛋白表达仍无明显变化(P>0.05)。在联合给予TP和Gly后,各观测指标的变化与联合给予TP和CQ后的结果类似,且两组各指标间比较均未见明显差异(P>0.05)。结论外源性雄激素可能通过上调自噬水平引发大鼠睾丸萎缩病理过程的发生,HMGB1在此过程中可能调节了自噬水平的改变。
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Exogenous androgen induces testicular atrophy in rats via autophagy effects
Abstract: Objective To investigate the effect and the possible mechanism of exogenous androgen in rat testicular atrophy. Methods 48 SD male rats were randomly divided into 6 groups and there were 8 rats in each group: control group (control), androgen (testosterone propionate, TP) group, androgen + chloroquine group (TP+CQ), androgen + glycyrrhizin group (TP+Gly), chloroquine (CQ, autophagy inhibitor) group and glycyrrhizin (Gly, HMGB1 inhibitor) group. The rats were treated with 21d respectively, then we measured the weight of the rats, the wet weight of the testis and the testicular index. The pathological changes of the rat testis were observed by HE staining and the expression of Beclin-1, LC3B-II, p62 and HMGB1 protein in the testicular tissue of rats was detected by Western-Blotting. Results After the intervention of TP, the rats\' testis wet weight and testicular index decreased (P<0.01). The testicular seminiferous tubules atrophied, the spermatogenic cells at all levels were disarranged with the number of layers decreasing, and the mature sperm was not found. The expression level of Beclin-1, LC3B-II and HMGB1 protein was up (P<0.05), and there was no statistical significance in the expression of p62 protein(P>0.05). After the combined administration of TP and CQ, the testis index of rats increased significantly (P<0.05); the damage of spermatogenic tubule and spermatogenic cells at all levels was obviously improved, and mature sperm was found; the expression level of Beclin-1, LC3B-II and HMGB1 protein was down (P<0.05), and there was no statistical significance in the expression of p62 protein(P> 0.05). After giving TP and Gly together, the change of the observed indexes is similar to that of the combined treatment of TP and CQ, and there was no significant difference between the two groups(P> 0.05). Conclusion Exogenous androgens may induce the pathogenesis of testicular atrophy in rats by increasing the levels of autophagy, and HMGB1 may regulate the change of autophagy during this process.
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