目的:PCOS模型动物卵巢细胞内PI3K信号通路的变化与卵巢内分泌功能关系密切,本研究旨在探索PCOS模型大鼠卵巢颗粒细胞中PI3K信号通路的变化趋势,并探讨隐丹参酮调节PCOS模型大鼠颗粒细胞功能的可能机制.方法:将从空白对照大鼠及PCOS模型大鼠获得的颗粒细胞分别分为空白组(空白对照组获取)、模型组(DHEA诱导PCOS模型大鼠获取)和隐丹参酮组(DHEA诱导PCOS模型大鼠获取,300 nM终浓度隐丹参酮处理24h)进行体外培养及相应药物的预后.对各组细胞进行凋亡比率、培养液激素水平、甾体激素合成酶表达水平、葡萄糖摄取能力及PI3K信号通路蛋白表达水平检测.结果:隐丹参酮能够显著缓解PCOS模型大鼠颗粒细胞葡萄糖摄取能力及培养液激素水平的异常;在显著提高卵巢颗粒细胞PI3K信号通路关键分子磷酸化水平的同时,降低了PCOS模型大鼠颗粒细胞甾体激素合成酶STAR及CYP17的表达水平.结论:隐丹参酮治疗PCOS模型大鼠生殖机能异常的机制与PI3K途径的激活密切相关.%Objective:To explore the changing tendency of PI3K pathway in the granulosa cells of PCOS model rats,and to discuss the possible mechanism of cryptotanshinone(CT) regulating granulosa cells in PCOS rats.Methods:Granulosa cells were divided into the blank control group(normal rats),the PCOS model group(DHEA intervened rats),CT group (DHEA intervened rats + 300 nM CT for 24 h).Apoptosis ratio,hormone level in cell-culture medium,the expression of steroid hormone synthetase,glucose uptake ability,and expression of PI3 K pathway were examined after in vitro culture and medications.Results:The abnormalities of cells' glucose uptake and steroid hormone level were adjusted by CT in PCOS rats.CT also decreased expressions of STAR and CYP17 with the activation of PI3K pathway.Conclusion:The mechanism of CT treating abnormal reproductive function in PCOS rats may be related to the activation of PI3K path
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