骨髓间充质干细胞（BMSCs）治疗早期股骨头坏死（ANFH）是骨科的研究热点。我们前期采用碱性成纤维细胞生长因子（bFGF）转染BMSCs治疗早期ANFH，疗效有限，坏死区氧化应激（OS）限制了BMSCs的存活和成骨。而帕金森病蛋白7（PARK7）可通过ERK1/2、Nrf2、ASK1和PI3K/Akt等通路发挥抗OS功能，我们预实验也证实PARK7可增强BMSCs抗OS。所以，我们推测：PARK7可通过上述通路增强BMSCs抗OS，促进其存活，从而提高BMSCs的移植效果。为验证此假说，我们拟采用基因过表达、ShRNA等技术，研究PARK7增强BMSCs抗OS的作用及机制；进而采用PARK7和bFGF基因共转染BMSCs构建组织工程骨修复早期ANFH模型，利用免疫荧光、Micro-CT等技术，观察BMSCs在体内的存活情况以及该组织工程骨的修复效果，为早期ANFH治疗提供新的思路和方法。

Bone marrow mesenchymal stem cells (BMSCs) treatment for early avascular necrosis of the femoral head (ANFH) has been a hotspot in orthopedics. BMSCs transfected by basic fibroblast growth factor (bFGF) have been used to treat early ANFH. However, its effectiveness is limited. Oxidative stress (OS) in the necrotic region restricts the survival and osteogenesis of BMSCs. Parkinson's disease protein 7 (PARK7) can fully play an anti-OS function via the pathways of ERK1/2, Nrf2, ASK1 and PI3K/Akt. Our preliminary experiment demonstrated that PARK7 can enhance the anti-OS of BMSCs. Therefore, our hypothesis is that PARK7 could enhance the anti-OS of BMSCs via these pathways and promote BMSCs survival, improving the transplantation effect of BMSCs. This study will investigate the role and function of PARK7 by gene overexpression and ShRNA. Furthermore, BMSCs co-transfected by PARK7 and bFGF will be used to repair the early ANFH model via constructing the tissue engineering bone. Immunofluorescence and Micro-CT will be used to observe the survival of BMSCs in vivo and the repair effectiveness of tissue engineering bone, providing new ideas and methods for early ANFH treatment.