由于肿瘤治疗手段的不断发展及发病年轻化的趋势，化疗性卵巢早衰（CIPOF）的发病率逐年上升，如何防治CIPOF已成为急需解决的问题。我们的前期研究证实了骨髓间充质干细胞（MSCs）能部分修复化疗药物损伤的卵巢结构及功能，尙达不到完全修复的效果。本项目以miR-21为切入点，通过检测临床CIPOF患者标本、动物模型及化疗药物诱导卵巢颗粒细胞凋亡模型中miR-21及其靶基因的表达特性，明确miR-21在CIPOF发病中的作用机制；构建miR-21慢病毒载体，转染MSCs，获得miR-21修饰的MSCs（miR-21-MSCs），探讨miR-21过表达对局部微环境下MSCs凋亡的影响；体内将miR-21-MSCs移植至动物模型卵巢组织，体外与化疗药物诱导凋亡的颗粒细胞共培养，观察miR-21联合MSCs治疗CIPOF的疗效。本项目对进一步阐明CIPOF的机制，提高疗效具有重要的科学及临床意义。

Because of the development of tumor treatment and the tendency to young people, the morbidity of chemotherapy induced premature ovarian failure(CIPOF) is gradually increasing, and how to prevent and treat it is the most urgent problem for clinician. Our previous investigation proved the partly repair effect of bone marrow derived mesenchymal stem cells(MSCs) for chemotherapy damaged ovarian construction and function, but the ovarian function can not return to normal. This project focuses on miR-21, the effect of miR-21 in mechanism of CIPOF is observed by examining the miR-21 and its target genes characters in clinical patients, rat models and chemotherapy induced granulose cells apoptosis models. Then we construct the slow viral carrier of miR-21, and transfect MSCs to get miR-21 modified MSCs(miR-21-MSCs). The MSCs apoptosis in CIPOF local micro-environment is examined in miR-21 over-expression condition. MiR-21-MSCs is transplanted to ovaries in CIPOF rat models in vivo and co-cultured with chemotherapy induced apoptotic granulose cells in vitro to investigate the effect of miR-21 combined with MSCs to CIPOF. The project is possess of important scientific and clinic meaning for CIPOF mechanism and treatment.