自噬
多囊卵巢
PI3K/AKT/mTOR通路
褪黑素
内分泌学
睾酮(贴片)
内科学
蛋白激酶B
卵泡期
细胞凋亡
卵巢
卵泡液
生物
信号转导
医学
细胞生物学
糖尿病
胰岛素抵抗
卵母细胞
胚胎
生物化学
作者
Fenfen Xie,Junhui Zhang,Muxin Zhai,Yajing Liu,Hui Hu,Zhen Yu,Junqiang Zhang,Shuai Lin,Dan Liang,Yunxia Cao
摘要
Emerging evidence has demonstrated that melatonin (MT) plays a crucial role in regulating mammalian reproductive functions. It has been reported that MT has a protective effect on polycystic ovary syndrome (PCOS). However, the protective mechanisms of MT remain poorly understood. This study aims to explore the effect of MT on ovarian function in PCOS and to elucidate the relevant molecular mechanisms in vivo and in vitro. Here, we first analysed MT expression levels in the follicular fluid of PCOS patients. A significant reduction in MT expression levels was noted in PCOS patients. Intriguingly, reduced MT levels correlated with serum testosterone and inflammatory cytokine levels in follicular fluid. Moreover, we confirmed the protective function of MT through regulating autophagy in a dehydroepiandrosterone (DHEA)-induced PCOS rat model. Autophagy was activated in the ovarian tissue of the PCOS rat model, whereas additional MT inhibited autophagy by increasing PI3K-Akt pathway expression. In addition, serum-free testosterone, inflammatory and apoptosis indexes were reduced after MT supplementation. Furthermore, we also found that MT suppressed autophagy and apoptosis by activating the PI3K-Akt pathway in the DHEA-exposed human granulosa cell line KGN. Our study showed that MT ameliorated ovarian dysfunction by regulating autophagy in DHEA-induced PCOS via the PI3K-Akt pathway, revealing a potential therapeutic drug target for PCOS.
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