Ki-67在肥胖PCOS大鼠模型卵巢颗粒细胞中的表达研究

Ki-67 Expression in Ovarian Granulosa Cells of Obese PCOS Rat Models

目的:探讨子宫内膜生存素Ki-67在肥胖多囊卵巢综合(PCOS)大鼠模型卵巢颗粒细胞中的表达。方法:分别在来曲唑(Letrozole)和脱氢表雄酮(DHEA)造模基础上加用高脂乳剂,建立肥胖PCOS动物模型,结合血清性激素、大鼠处死时体重增加幅度及脏器指数改变进行模型验证,选用免疫组织化学法检测大鼠模型卵巢组织卵泡颗粒细胞中Ki-67的表达。结果:模型建立成功。Letrozole模型组和DHEA模型组Ki-67积分光密度总和、平均灰度均值显著低于空白对照组(P<0.05),此外,Letrozole肥胖模型组和DHEA肥胖模型组Ki-67积分光密度总和、平均灰度均值极显著低于空白对照组和高脂模型组(P<0.01);Letrozole肥胖模型组Ki-67平均灰度均值显著低于Letrozole模型组(P<0.05),DHEA肥胖模型组Ki-67平均灰度均值显著低于DHEA模型组(P<0.05),差异有统计学意义。结论:Ki-67在PCOS大鼠模型卵巢的卵泡颗粒细胞中表达降低可能是PCOS发生发展的重要原因,且Ki-67在肥胖PCOS大鼠模型卵巢卵泡颗粒细胞中表达降低更明显。

Objective： To study the expression of endometrial survival Ki- 67 in the ovarian granulosa cells of the obese Polycystic Ovary Syndrome（ PCOS） rat models. Methods： The obesity PCOS rat models were built respectively with high fat emulsion on the basis of Letrozole and（ Dehydroepiandrosterone） models. The models were verified by the weight growth rate when rats were killed,the serum sex hormone levels and the change of organ index. Immunohisto chemical method was chosen to detect the expression of Ki- 67 in the ovarian tissue granulosa cells of rat models. Results： Models were set up successfully. Both of the integral optical density and the average gray scale value of Ki- 67 in Letrozole group and DHEA group were significantly lower than that of the blank control group（ P 〈 0. 05）. Besides,both the integral optical density and the average gray scale value of Ki- 67 in Letrozole obese group and DHEA obese group were significantly lower than those of the blank control group and the high fat emulsion group（ P 〈 0. 01）. The Ki- 67 average gray scale value in Letrozole obese group was significantly lower than that of the Letrozole group（ P 〈 0. 05）. The Ki- 67 average gray scale value in DHEA obese group was significantly lower than that of the DHEA group（ P 〈 0. 05）. The differences were statistically significant. Conclusion： It can be inferred that the expression of Ki- 67 reduced in the ovarian follicle granulosa cells of the PCOS rat models were likely to be the important reason for occurrence and development of the PCOS and it was more obvious in the obese PCOS rat models.