SMAD3敲除对雄性小鼠生殖功能的影响

Effect of SMAD3 knockout on the reproduction of male mice

目的探讨SMAD3缺失对雄性小鼠生殖功能的影响。方法野生型雌性小鼠分别与基因敲除(实验组)及野生型(对照组)雄性小鼠配对;睾丸常规石蜡包埋、切片并进行HE、TUNEL染色;对附睾精子进行形态、动力学分析等。结果实验组受孕率为92%,对照组受孕率100%;实验组每窝仔鼠数目为(5.45±0.78)只,存活率(87±19)%;对照组每窝仔鼠(6.01±1.03)只,存活率(97±15)%。不同发育阶段(7、18及90 d)基因敲除小鼠的睾丸与同龄野生型相比,组织学结构未见明显异常,生精细胞凋亡未见明显增加。其精子形态正常,数量及活力与野生型相比无显著下降。结论SMAD3敲除对雄性小鼠生殖功能无明显影响,提示SMAD3在睾丸中的功能是可以被替代的。

Objective To investigate the effect of SMAD3 knockout on the reproduction of male mice. Methods Adult wild type females were mated with knockout or wild type males; Testis were performed with HE and TUNEL staining; Cauda epididymal sperms were counted and analyzed with morphology and motility. Results Wild-type / knock-out pairs resulted in a pregnancy rate of 92% with an average litter size of 5.45 ± 0. 78 and a live birth rate of （87 ±19）%. In the wild-type / wild-type pairs, 100% females were pregnant, the litter size was 6.01 ± 1.03, and the live rate was （97 ±15）%, there was no significant difference between the two groups. Histological analysis showed a relatively normal spermatogenesis in knockout testis, and TUNEL analysis did not demonstrate more apop- totic cells in knock-out testis. The cauda epididymal sperm number was normal, and there was no obvious difference in the sperm motility and morphology in the knock-out males. Conclusion The function of SMAD3 can be compensated in male reproduction.