摘要
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 n M终浓度隐丹参酮处理24 h)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 PI3 K to discuss the possible mechanism of cryptotanshinone （CT） pathway in the granulosa cells of PCOS model rats, and regulating granulosa ceils in PCOS rats. Methods： Granulosa ceils 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 PI3K pathway were examined after in vitro cul- ture 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- way.
作者
匡洪影
马珂昕
李威
陈静
孙荣
张跃辉
KUANG Hong- ying MAKe- xin LI Wei CHEN Jing SUN Rong ZHANG Yue- hui(The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin 150040, China Heilongfiang University of Chinese Medicine ,Harbin 150040, China)
出处
《中医药学报》
CAS
2017年第5期40-44,共5页
Acta Chinese Medicine and Pharmacology
基金
国家自然科学基金青年基金(81503610)
黑龙江省自然科学基金面上项目(H2016083)
哈尔滨市科技创新人才研究专项基金(RC2015QN00309)
黑龙江省普通本科高等学校青年创新人才培养计划(UNPYSCT-2016076)
黑龙江省留学回国人员择优资助(LBH-Z11006)
