Weng Yashuang, Zhang Wenbo, Qu Fan, Deng Zehua, Zhang Xiaodan, Liu Shuang, Wei Hongwei, Hao Tiantian, Gao Longwei, Zhang Meijia, Chen Yuezhou
The Innovation Centre of Ministry of Education for Development and Diseases, School of Medicine, South China University of Technology, Guangzhou, China.
Center for Reproductive Medicine, Zhongshan City People's Hospital, Zhongshan, China.
Mol Hum Reprod. 2025 Apr 3;31(2). doi: 10.1093/molehr/gaaf007.
The activation of dormant primordial follicles is a promising method to improve the fertility of premature ovarian insufficiency (POI) patients. Many experiments from both human and animal studies suggest that human platelet-rich plasma (hPRP) may restore ovarian function and promote follicle growth. However, the underlying mechanisms remain unclear. In the current study, our results demonstrate that hPRP significantly increased the number of growing follicles and promoted the proliferation of granulosa cells in cultured mouse ovaries. hPRP also significantly increased the protein levels of phosphorylated protein kinase B (p-Akt) and forkhead box O3a (p-FOXO3a), as well as the number of oocytes with FOXO3a nuclear export in cultured mouse ovaries. Immunofluorescence results showed that in vitro treatment with hPRP significantly increased the fluorescence intensity of p-Akt in oocytes. The inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway by LY294002 blocked the hPRP-induced increase in the number of growing follicles in cultured mouse ovaries. Furthermore, hPRP injected i.p. or added to the medium significantly increased the number of growing follicles and the protein levels of p-Akt in the ovaries of newborn mice and in cultured human ovarian tissues. Taken together, our findings from mouse and human experiments indicate that hPRP promotes the activation of primordial follicles through the PI3K/Akt signaling pathway in oocytes.
激活休眠的原始卵泡是提高卵巢早衰（POI）患者生育能力的一种有前景的方法。来自人类和动物研究的许多实验表明，富含血小板的血浆（hPRP）可能恢复卵巢功能并促进卵泡生长。然而，其潜在机制仍不清楚。在本研究中，我们的结果表明，hPRP显著增加了培养的小鼠卵巢中生长卵泡的数量，并促进了颗粒细胞的增殖。hPRP还显著增加了培养的小鼠卵巢中磷酸化蛋白激酶B（p-Akt）和叉头框O3a（p-FOXO3a）的蛋白水平，以及具有FOXO3a核输出的卵母细胞数量。免疫荧光结果显示，用hPRP进行体外处理显著增加了卵母细胞中p-Akt的荧光强度。LY294002对磷脂酰肌醇3-激酶（PI3K）/Akt通路的抑制阻断了hPRP诱导的培养小鼠卵巢中生长卵泡数量的增加。此外，腹腔注射hPRP或添加到培养基中显著增加了新生小鼠卵巢和培养的人卵巢组织中生长卵泡的数量以及p-Akt的蛋白水平。综上所述，我们在小鼠和人类实验中的发现表明，hPRP通过卵母细胞中的PI3K/Akt信号通路促进原始卵泡的激活。
