骨髓间充质干细胞（BMSCs）在激素性股骨头坏死（ESANFH）治疗中发挥重要潜能，但移植后大量细胞凋亡极大限制了治疗效果。长链非编码RNA（lncRNAs）具有广泛的生物学功能，新近研究发现lncRNA-Meg3通过调节氧化应激参与凋亡，且具有可调控性。缺血/缺氧诱导BMSCs凋亡与氧化应激关系密切。巨噬细胞迁移抑制因子（MIF）通过调节氧化应激反应，发挥抗凋亡作用。前期预实验提示：缺血/缺氧条件下，BMSCs中lncRNA-Meg3表达明显升高，可被MIF所抑制。因此，我们推测MIF可调控lncRNA-Meg3降低BMSCs凋亡，并且联合新型PEG微冰胶，利用其微创可注射性、优异的力学性质和防细胞渗漏特点，进行兔ESANFH模型体内移植治疗。同时体外探究Wnt/β-catenin信号通路在MIF调节lncRNA-Meg3抗凋亡中的关键作用，为ESANFH损伤提供微创治疗新理念和新策略。

Bone mesenchymal stem cells (BMSCs) based therapies have had positive outcomes in treatment of Early steroid-induced avascular necrosis of femoral head (ESANFH). However, lots of BMSCs went apoptosis, reducing their ability to contribute to ESANFH injury repair. Long noncoding RNAs (lncRNAs) regulate diverse biological processes. Latest research found that lncRNA-Meg3 took part in cellular apoptosis though modulating cellular oxidative stress, and can be modulated. Apoptosis induced by hypoxia/serum deprivation is closely related with cellular oxidative stress in BMSCs. Macrophage migration inhibitory factor (MIF) can modulate oxidative stress to resist cellular apoptosis in many kinds of cells. In our previous experiments, we found that the expression of lncRNA-Meg3 was increased under hypoxia/serum deprivation condition when compared with normal, while the expression of lncRNA-Meg3 was inhibited by exogenous MIF. Here, we suggest that exogenous MIF may ameliorate the BMSCs apoptosis induced by hypoxia/serum deprivation through modulating lncRNA-Meg3, Previous inventing novel injectable microcryogels delivery, which have confirmewd its excellent characteristics of minimally invasive injectable, provided mechanically strength and avoided cell leaking will be loaded and improve effect of therapy of ESANFH in vivo. In vitro, we culture rabbit BMSCs, and research Wnt/β-catenin signaling pathway function in MIF conferring resistance apoptosis through modulating lncRNA-Meg3. The purpose is to provide a new idea and therapeutic implications of minimally invasive treatment for ESANFH.