氧化应激与细胞自噬凋亡对卵巢早衰调控的研究进展  

Advances on Regulation of Premature Ovarian Failure by Oxidative Stress and Autophagy Apoptosis

作　　者：杨开锋 李兰 周虹 肖小芹[1] 刘慧萍[1] YANG Kaifeng;LI Lan;ZHOU Hong;XIAO Xiaoqin;LIU Huiping(Hunan University of Chinese Medicine,Changsha,Hunan 410208,China)

机构地区：[1]湖南中医药大学,湖南长沙410208

出　　处：《湖南中医药大学学报》2021年第5期809-814,共6页Journal of Hunan University of Chinese Medicine

基　　金：湖南省自然科学基金面上项目(2020JJ4469);湖南省教育厅重点项目(19A377);湖南省研究生科研创新项目(CX20200793);湖南省教育厅创新平台开放基金项目(18K069)。

摘　　要：卵巢早衰是导致女性不孕的主要原因,研究证实氧化应激与卵巢早衰密切相关。氧化应激可以通过不同途径介导细胞自噬和凋亡的发生,在卵巢当中,正常浓度的活性氧的有助于卵巢的发育和排卵,而过多的活性氧则会导致卵巢颗粒细胞和卵母细胞的过度凋亡,从而引发卵巢早衰。因此,减少卵巢的氧化应激,防止颗粒细胞过度凋亡,可为临床防治卵巢早衰提供重要的研究方向。Nrf2-ARE信号通路是目前发现的最为重要的内源性抗氧化应激通路,通过对Nrf2-ARE信号通路与卵巢早衰关系的总结,为卵巢早衰发病机制的进一步研究提供参考。Premature ovarian failure is the main cause of female infertility.It has been confirmed that oxidative stress is closely related to premature ovarian failure.Oxidative stress can mediate autophagy and apoptosis through different pathways.In the ovary,normal concentration of reactive oxygen species contributes to ovarian development and ovulation,while excessive reactive oxygen species will lead to excessive apoptosis of ovarian granulosa cells and oocytes,thus triggering premature ovarian failure.Therefore,reducing oxidative stress and preventing excessive apoptosis of granulosa cells in the ovary can provide an important research direction for clinical prevention and treatment of premature ovarian failure.Nrf2-ARE signaling pathway is the most important endogenous anti-oxidative stress pathway found at present,and the relationship between Nrf2-ARE signaling pathway and premature ovarian failure is summarized to provide a reference for further study of the pathogenesis of premature ovarian failure.

关 键 词：卵巢早衰 氧化应激 Nrf2-ARE信号通路 细胞自噬 细胞凋亡 

分 类 号：R285[医药卫生—中药学] R711[医药卫生—中医学]