多囊卵巢综合征患者卵巢黄素化颗粒细胞瘦素信号转导分子STAT3磷酸化表达的研究

目的检测多囊卵巢综合征(PCOS)患者卵巢黄素化颗粒细胞瘦素信号转导子和活化子STAT3磷酸化(p-STAT3)水平,并观察瘦素体外对培养卵巢黄素化颗粒细胞p-STAT3水平的影响,探讨瘦素在PCOS发病机制中的作用。方法选择行体外受精-胚胎移植(IVF-ET)治疗的肥胖型PCOS患者(肥胖PCOS组)、非肥胖型PCOS患者(非肥胖PCOS组)、排卵功能正常和单纯输卵管因素不育的肥胖(肥胖对照组)及正常体重妇女(正常对照组)各15例。采用免疫印迹技术检测卵巢黄素化颗粒细胞p-STAT3水平。同时将正常人卵巢黄素化颗粒细胞行体外培养,分别加入不同浓度的瘦素(0、10、100、1,000 ng/ml)培养48 h,观察瘦素体外对人卵巢黄素化颗粒细胞p-STAT3水平的影响。结果(1)肥胖型PCOS组、肥胖对照组、非肥胖PCOS组和正常对照组卵巢黄素化颗粒细胞p-STAT3水平分别为(24.28±0.51)、(21.31±1.32)、(11.69±0.67)、(9.03±0.20),实验组间比较有显著性差异(P<0.05),其中肥胖型PCOS组p-STAT3表达水平最高,其次依次为肥胖对照组、非肥胖PCOS组和正常对照组。各组之间两两比较,均有显著性差异(P<0.05)。(2)加入瘦素培养48 h后,卵巢黄素化颗粒细胞p-STAT3水平随瘦素浓度升高而增高,呈浓度依赖性,至瘦素浓度达到100 ng/ml时,p-STAT3水平达到高峰,随后呈下降趋势。结论瘦素通过介导JAK2/STAT3信号途径可能参与了肥胖型PCOS的发病机制。

Study on expression of STAT3 phosphorylation in granulosa cells of patients with polycystic ovary syndrome

Objective: To detect the level of signal transduction molecule STAT3 phosphorylation(p-STAT3) in granulosa cells of patients with polycystic ovary syndrome(PCOS),and the influence of leptin at different concentrations on the level of p-STAT3 in granulosa cells in vitro.Methods: Granulosa cells were collected from the puncture fluid of follicle of 15 obese and 15 non-obese PCOS patients,and 15 obese and 15 non-obese women without PCOS who were undergoing IVF-ET.The granulosa cells from 10 normal women were cultured in the medium supplemented with different concentrations of leptin(0,10,100,1,000 ng/ml) for 48 h.Western blot was used to determine the levels of p-STAT3 in granulosa cells.Results:(1) The levels of p-STAT3 in granulosa cells of obese PCOS patients,obese control group,non-obese PCOS patients and non-obese control group were 24.28±0.51,21.31±1.32,11.69±0.67 and 9.03±0.20,respectively,with significant difference between groups(P<0.05).(2) When granulosa cells werestimulated in vitro by leptin for 48 h,the levels of p-STAT3 increased in a dose-dependent manner.The levels reached the peak when the concentration of leptin was 100 ng/ml,and then began to decrease.Conclusion: From the results of this study,we can conclude that leptin may be involved in physiopathology of obese PCOS through JAK2/STAT3 signal transduction pathway.