高雄激素血症多囊卵巢综合征（PCOS）女性卵泡颗粒细胞自噬水平上升引发卵泡闭锁,但是颗粒细胞自噬上升的机制不清。我们前期研究发现（1）高雄PCOS模型小鼠卵巢组织RasGRP1表达显著低于对照小鼠；（2）卵泡颗粒细胞沉默RasGRP1后， LC3增加；（3）高雄激素血症PCOS女性颗粒细胞高表达靶向调控RasGRP1的miR-221/222。然而miR-221/222在PCOS颗粒细胞自噬的作用未知，结合前期结果，我们提出高雄激素导致miR-221/222升高，抑制RasGRP1表达，促进颗粒细胞自噬的假说。本研究拟通过在卵泡颗粒细胞和高雄PCOS模型小鼠中研究miR-221/222调控RasGRP1抑制mTOR活化的具体分子机制，阐明卵巢局部高雄激素环境miR-221/222靶向RasGRP1在颗粒细胞自噬的调控模式，旨在为高雄激素血症PCOS患者的促排卵治疗提供新的思路。

The increased level of autophagy in follicular granulosa cells(GCs) in polycystic ovary syndrome (PCOS) women with hyperandrogenism induces follicular atresia. But the mechanism of the high level of autophagy in GCs is unknown.Our previous work found that (1) the expression level of RasGRP1 in ovarian tissue of prenatally androgenized mice was significantly lower than that of control mice; (2)LC3 protein increased after silencing RasGRP1 in KGN cells;(3)the expression of miR-221/222 is higher in GCs of PCOS women with hyperandrogenism than that of normal control, and miR-221/222 inhibits the post-transcriptional level of RasGRP1.However, the role of miR-221/222 in GCs autophagy of PCOS is unknown. Based on our previous results, we propose that high androgen causes the increased level of miR-221/222, which inhibits RasGRP1 expression, and promotes GCs autophagy.This study intends to find the specific molecular mechanism of the expression of RasGRP1 regulated by miR-221/222 and inhibiting mTOR activation by using follicular GCs and prenatally androgenized mice.We intend to clarify the regulatory mode of miR-221/222 targets RasGRP1 in follicle GCs in the high level of androgen environment, and aim to provide new ideas for the clinical treatment of PCOS patients with hyperandrogenism.