肿瘤治疗引起化疗性卵巢早衰/功能不全(POF/POI)的发病率逐年上升，间充质干细胞防治POF/POI已成为热点，但急需明确防治效果与机制。课题组和已有报道显示胎盘间充质干细胞(PMSCs)移植可起到抗氧化和改善卵巢功能的作用，组学数据和前期预实验证实hPMSC移植可抑制化疗受损POF卵巢的过度自噬作用而提高修复效果，但机制尚未完全阐明。在以往基础上本研究拟采用环磷酰胺致POF大鼠hPMSC移植、卵巢皮质和原始卵泡与hPMSCs共培养模型，hPMSCs旁分泌和外泌体系统阻断、自噬抑制剂与双荧光mRFP-eGFP-LC3体系等方法，阐明hPMSCs对损伤卵巢中自噬抑制和稳态平衡的影响，进一步探讨hPMSCs通过mTOR激活和P62泛素化水平降低而抑制自噬的机制，明确hPMSCs在调节细胞存活、重启卵泡发育和激素分泌等生殖功能方面的保护优势，为化疗性卵巢功能衰竭患者的临床治疗提供实验基础。

Chemotherapy inevitably leads to premature ovarian failure/insufficiency(POF/POI) in young women. Currently it cannot find a satisfactory control strategy to prevent chemotherapy-induced ovary damage. Human placenta-derived mesenchymal stem cells (hPMSCs)have higher expression of HGF, IGF-II and PDGF-aa than bone marrow adipose-derived MSCs. To investigate whether hPMSCs-secreting cytokines act as molecular basis to attenuate chemotherapy-induced ovarian injury, we will evaluate the ovarian function with unilateral ovary of POF/POI rats model, natural recovery group hPMSCs transplantation group and primordial follicles and mesenchymal cells co-cultivated model. It was found that hPMSCs transplantation could inhibit ovarian cell death induced by continuous autophagy. Bioinformatics analysis of RNA-seq data revealed that growth factor-mediated mTOR pathway activation and decreased ubiquitination level to inhibit autophagy as a potential mechanism. Therefore, we will investigate the differences in autophagy associated protein expression, changes in autophagy level and the association with mTOR activation and ubiquitination level of injured cells by blocking the paracrine and exosome systems of hPMSCs.We further discuss the effect and mechanism of hPMSCs on the inhibition of autophagy and homeostasis in damaged ovaries, and to clarify the protective advantages of hPMSCs in regulating the survival of functional cells, restarting the development of a pool of primordial follicles, hormone secretion and other reproductive functions.