补肾方药通过PI3K/Akt/NF-κB信号通路抑制卵巢颗粒细胞凋亡的作用机制思考

Thoughts on the mechanism of kidney-tonifying prescriptions regulating PI3K/Akt/NF-κB signaling pathway to inhibit ovarian granulosa cell apoptosis

摘要:

早发性卵巢功能不全（premature ovarian insufficiency，POI）作为常见的生殖内分泌疾病，危害女性的生殖健康和生活质量。研究发现POI的发病机制与卵巢颗粒细胞过度凋亡相关。颗粒细胞过度凋亡会使卵泡提前闭锁，导致卵巢功能下降。同时，PI3K/Akt/NF-κB信号通路及凋亡蛋白参与凋亡过程。补肾方药能够抑制颗粒细胞凋亡，改善卵巢功能，临床疗效显著，并且对PI3K/Akt/NF-κB信号通路有调控作用。因此，本文结合相关文献报道，推测补肾方药可能通过调控PI3K/Akt/NF-κB信号通路抑制卵巢颗粒细胞凋亡治疗POI，为基础研究及临床诊疗提供思路与方法。

Abstract:

As a common reproductive endocrine disease, premature ovarian insufficiency (POI) endangers women’s reproductive health and quality of life. Excessive apoptosis of ovarian granulosa cells has been confirmed to affect the development of follicles, which may be the pathogenesis of POI. It has been found that apoptosis of granulosa cells is related to PI3K/Akt/NF-κB signal pathway and the expression of apoptotic protein. Kidney-tonifying prescriptions can inhibit granulosa cell apoptosis, improve ovarian function, and regulate the expression of signal molecules related to PI3K/Akt/NF-κB signaling pathway. Therefore, combined with relevant literature reports, it is speculated that kidney-tonifying prescriptions may inhibit ovarian granulosa cell apoptosis by regulating PI3K/Akt/NF-κB signaling pathway to provide ideas and methods for basic research and clinical diagnosis and treatment of POI.