Objective:To explore the role of icariin in the animal models of the cyclophosphamide-induced rat testis spermatogenic failure,and study the effects of icariin on the hypothalamus-pituitary-testicular axis.Methods:Rats were divided into blank control group,negative control group,model group and icariin treatment group.H-E staining was used to observe the morphological structural changes in testicular tissue.TUNEL method was used to detect the apoptosis of testicular germ cells.Serum testosterone,follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were detected by radioimmunoassay.GnRH nerve fibers in median eminence of the rat hypothalamus were detected by SABC immunohistochemistry.Results:H-E staining observation of testicular tissue in model group rats showed the testis seminiferous tubule diameter narrowed,the spacing between seminiferous tubules widened,and the seminiferous epithelium became thinner.The number of germ cells decreased,and sperm was rarely found in seminiferous tubules.Compared with blank control group,there was significant change in seminiferous tubules.Compared with model group,treatment group showed signs of thickening seminiferous tubule epithelium and significant increase of seminiferous tubules with sperms.Model group showed obvious increase of germ cell apoptosis in testicular seminiferous tubules compared with blank control group.Treatment group showed obvious decrease of germ cell apoptosis in seminiferous tubules compared with model group.Serum testosterone of the model group was significantly decreased compared with the blank control group;serum testosterone of treatment group was significantly increased compared with model group.There was no significant difference in serum FSH and LH level between these groups.GnRH-positive fibers in the median eminence of model group showed signs of increased GnRH-positive fibers,deeper staining and significant change in optical density compared with blank control group.Compared with model group,treatment group showed signs of reduced GnRH-positive fibers and lighter staining.There were no significant differences in all the parameters between the negative control group and the blank control group.Conclusion:Icariin improves the testicular seminiferous tubule structure,and promotes spermatogenesis and testosterone secretion of Leydig cells.Icariin reduces the apoptosis of the testicular germ cells and the content of GnRH in the median eminence.%目的:探讨淫羊藿苷在环磷酰胺诱导的大鼠睾丸生精障碍动物模型中的作用,研究淫羊藿苷对下丘脑-垂体-睾丸轴的影响.方法:大鼠分为空白对照组、阴性对照组、模型组、淫羊藿苷治疗组;H-E染色观察睾丸组织结构变化,TUNEL检测睾丸生殖细胞凋亡,放射免疫法检测血清睾酮、卵泡刺激素(FSH)、黄体生成素(LH),SABC免疫组织化学研究下丘脑正中隆起促性腺激素释放激素(GnRH)神经纤维.结果:睾丸H-E染色切片观察显示模型组睾丸生精小管直径缩小,间距增宽,生精上皮变薄,生殖细胞数量减少,生精小管多未见精子形成,与空白对照组比较其生精小管结构变化显著;治疗组与模型组比较生精小管壁增厚,含有精子的生精小管明显增多.模型组与空白对照组比较,睾丸生精小管中生殖细胞凋亡显著增多;治疗组与模型组比较生精小管中生殖细胞凋亡数量明显减少.血清睾酮检测结果显示模型组与空白对照组比较血清睾酮明显降低;治疗组与模型组比较其血清睾酮明显增加;血清FSH、LH水平各组间无差异.与空白对照组比较,模型组正中隆起GnRH阳性纤维增多,染色深,光密度显著增高;治疗组与模型组比较其GnRH阳性纤维明显减少,染色浅.结论:淫羊藿苷具有改善睾丸生精小管结构、减少生殖细胞凋亡、促进精子发生和间质细胞分泌睾酮的功能,降低GnRH在正中隆起的蓄集.
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