论文部分内容阅读
目的:探讨米非司酮抑制卵泡发育的可能机制。方法:收集腹腔注射60 IU孕马血清促性腺激素(PMSG)的未成年SD雌性大鼠的卵巢颗粒细胞(GC)进行体外培养,采用电子显微镜对未处理的颗粒细胞进行鉴定,运用免疫细胞化学法观察不同浓度米非司酮(10-6 mol/L、10-5 mol/L、10-4 mol/L)对GC中Fas表达的影响。结果:原代培养大鼠卵巢GC活细胞数可达80%-85%;免疫细胞化学结果显示GC中Fas蛋白表达随米非司酮处理剂量的增加而增强,阳性表达率10-6 mol/L组(0.290±0.065)、10-5 mol/L组(0.364±0.075)和10-4 mol/L组(0.557±0.067)与对照组(0.194±0.082)之间均有统计学差异(P<0.01),各组间也均有差异(P<0.05)。结论:调节颗粒细胞表面凋亡因子Fas蛋白的表达可能是米非司酮诱导颗粒细胞凋亡、抑制卵泡发育的机制之一。
Objective: To investigate the possible mechanisms by which mifepristone inhibits follicular development. Methods: Ovary granulosa cells (GCs) of female SD rats were injected intraperitoneally with 60 IU of pregnant mare serum human gonadotrophin (PMSG) and cultured in vitro. Untreated granulosa cells were identified by electron microscopy. Immunocytochemistry The effects of different concentrations of mifepristone (10-6 mol / L, 10-5 mol / L, 10-4 mol / L) on the expression of Fas in GC were observed. Results: The number of viable cells in ovaries of primary cultured rats reached 80% -85%. The results of immunocytochemistry showed that the expression of Fas protein in GC increased with the increase of mifepristone, and the positive expression rate was 10-6 mol / There was a significant difference between the control group (0.290 ± 0.065), the 10-5 mol / L group (0.364 ± 0.075) and the 10-4 mol / L group (0.557 ± 0.067) and the control group <0.01). There were also differences among the groups (P <0.05). Conclusion: Regulating the expression of Fas protein on granulosa cells may be one of the mechanisms by which mifepristone induces granulosa cell apoptosis and inhibits follicular development.