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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 investigate the expression of endometrial survivin Ki-67 in ovarian granulosa cells of obese polycystic ovary syndrome (PCOS) rat model. Methods: The model of obese PCOS was established by adding high-fat emulsion to Letrozole and DHEA respectively. Combined with serum hormone, weight gain and organ index Change the model validation, immunohistochemistry was used to detect the expression of Ki-67 in rat ovarian granulosa cells. Results: The model was established successfully. Ki-67 integral optical density and mean gray value of Letrozole model group and DHEA model group were significantly lower than those of blank control group (P <0.05). In addition, the Ki-67 integral optical density of Letrozole model group and DHEA model group, (P <0.01). Mean Ki-67 mean gray value in Letrozole model group was significantly lower than that in Letrozole model group (P <0.05), and Ki-67 in DHEA model group was significantly lower than that in model group -67 average gray mean value was significantly lower than DHEA model group (P <0.05), the difference was statistically significant. Conclusions: The decreased expression of Ki-67 in follicular granulosa cells of ovariectomized PCOS rats may play an important role in the development of PCOS, and the expression of Ki-67 in ovarian follicular granulosa cells of obese PCOS rats is more obviously reduced.