颗粒细胞凋亡影响多囊卵巢综合征患者卵泡闭锁的研究进展

Research progress of granulosa cell apoptosis affecting follicular atresia in patients with polycystic ovary syndrome

多囊卵巢综合征(PCOS)通过多种复杂的机制影响着女性生育能力,如胰岛素抵抗(IR)、氧化应激、慢性炎症,以及随之而来的高雄激素血症、脂肪因子分泌紊乱等可改变颗粒细胞生存的外部环境,在颗粒细胞受到这些外部因素刺激时,导致B细胞淋巴瘤2(Bcl-2)家族中抗凋亡成员与促凋亡成员比例失调,激活细胞内凋亡通路,主要由线粒体途径介导,通过增加线粒体外膜的通透性,促进线粒体释放多种促凋亡蛋白质如细胞色素c(Cytc),进入胞质的Cyt c随后形成凋亡小体进而级联激活胱天蛋白酶(caspase)家族,使颗粒细胞发生凋亡。一旦颗粒细胞发生凋亡,PCOS患者体内卵泡丧失生物学功能并且卵泡内细胞之间的调控失衡,促使卵母细胞和卵泡膜细胞发生凋亡,最终导致卵泡发生闭锁。本文查阅了大量相关文献,旨在探讨PCOS患者颗粒细胞凋亡与卵泡闭锁的关系及其作用机制。

Polycystic ovary syndrome(PCOS)affects female fertility through a variety of complex mechanisms,such as insulin resistance(IR),oxidative stress,chronic inflammation,and subsequent hyperandrogenemia,adipokine secretion disorder and other factors,changing the external environment for the survival of granular cells.When granulosa cells are stimulated by these external factors,the proportion of anti-apoptotic and pro-apoptotic members in the B-cell lymphoma 2(Bcl-2)family is disproportionally affected,and the intracellular apoptosis pathway is activated,mainly mediated by the mitochondrial pathway.By increasing the permeability of the mitochondrial outer membrane,the mitochondria promote the release of a variety of pro-apoptotic proteins such as cytochrome c(Cyt c).Entering the cytoplasm,Cyt c then forms apoptotic corpuscles,which cascade activation of the caspase family and apoptosis of granulosa cells.Once granulosa cell apoptosis occurs,the follicles in PCOS patients lose their biological function and the regulation between the cells in the follicle is unbalanced,which promotes the apoptosis of oocytes and follicular membrane cells,and eventually leads to the atrexia of follicles.In this paper,we reviewed a large number of relevant literatures to explore the relationship between granulosa cell apoptosis and follicular atresia in PCOS patients and its mechanism.