目的 研究多囊卵巢综合征（PCOS）胰岛素抵抗（IR）与非抵抗患者子宫内膜的PI3K/AKT/GSK3信号通路蛋白表达情况；探讨胰岛素在PCOS患者子宫内膜病变的作用机制。方法 以2006年3月至2010年5月北京天坛医院妇产科门诊治疗的34例PCOS患者为实验组，以同期因输卵管因素不孕行诊刮术的非PCOS患者30例为对照组。实验组患者行OGTT、INS实验及性腺6项测定，根据是否存在IR将PCOS患者分为I组(IR组)和II组(非IR组)。对实验组和对照组患者子宫内膜石蜡标本应用免疫组化方法测定PI3K(磷脂酰肌醇-3激酶)、p-AKT(PPKB，磷酸化蛋白激酶B)、GSK3(糖原合成酶激3)的表达。结果 PCOS患者的PI3K表达水平要明显高于对照组（P=0.000，0.003），其中PCOS I组最高（P=0.022)。在p-AKT表达上，PCOS患者要明显高于对照组（P=0.011，0.000），其中以PCOS I组最高（P=0.002），而在GSK3表达上，PCOS I组，II组和对照组三组之间差异无统计学意义(P>0.05）。结论 胰岛素信号通路PI3K、p-AKT可能是IR PCOS患者子宫内膜病变的信号转导通路。

Abstract: Objective To investigate the expression of PI3K/AKT/GSK3 signal pathways of endometrial lesions in Polycystic Ovary Syndrome (PCOS) patients with insulin resistance and non-insulin resistance and to determine the mechanism of insulin in endometrial lesions in PCOS patients. Methods 34 cases of PCOS patients as treatment group and 30 cases of patients with sterility due to oviduct diseases and treated through uterus curettage as control group were selected and involved in this study. The OGTT, INS experiment and 6 items of sex glands were determined in patients of treatment group, and divided PCOS patients in to groupⅠ (insulin resistance group) and groupⅡ (Non-insulin resistance group) depending on whether existed insulin resistance. The expression of PI3K (phosphatidylinositol 3-kinase), p-AKT (PPKB, phosphorylated protein kinase B) and GSK3 (glycogen synthase kinase 3) in paraffin section specimen of endometrial were determined by immunohistochemical methods. Results The express level of PI3K in PCOS patients were higher than that in control group (P<0.01) with the highest level in group I. The express level of p-AKT in PCOS patients were higher than that in control group (P<0.01) with the highest level in group I. There were no significant difference among the express level of GSK3 in group I, groupie and control group (P>0.05). Conclusion Insulin signal pathways PI3K and p-AKT may be the signal transduction pathways of endometrial lesions in PCOS patients with insulin resistance.