수컷 랫드에서 졍관절제술에 의한 생식세포의 Apoptosis

The pathological mechanism of impaired spermatogenesis after vasectomy has not been completely investigated. In this study, we examined pathological changes of the testis and the Fas-Fas ligand (FasL) mediated signaling pathway in apoptotic germ cell death after vasectomy in rats. Ten-weeks old Sprague-Dawley rats were underwent bilateral vasectomy and sacrificed after 1 day, 2 days, 3 days, 5 days, 1 week, 2 weeks, and 4 weeks of surgery and the testes were removed. Histopathological evaluation of spermatogenesis was performed by hematoxylin-eosin and periodic acid-Schiff-hematoxylin staining. To elucidate the pathophysiology of seminiferous tubule damage, terminal dUTP nick end labeling staining, electrophoresis assay of DNA fragmentation, and Western blotting analysis for Fas-FasL were performed. Relative weights of testes were decreased from 5 days after vasectomy. Germ cell degeneration were first found in the spermatogonia and spermatocytes at stages I-VI, and XII-XIV seminiferous tubules. Mean incidence of apoptotic germ cells after vasectomy progressively increased to peak in 5 days, and then gradually decreased to the control levels in 2 weeks after vasectomy. The expression of Fas-FasL reached maximum level at 5 days after vasectomy and then declined. In conclusion, impaired spermatogenesis after vasectomy associated with an increase in germ cell apoptasis, which is partly mediated by the activation of Fas-FasL.