激素型股骨头坏死发生过程中，成骨细胞分化因子osteocalcin(OCN)表达显著下降。维生素K(VK)调节OCN羧基化过程，MiR-133a在OCN功能化过程中发挥了重要作用。我们预实验发现VK可在体外促进骨髓间充质干细胞(BMSC)的成骨分化;还可预防糖皮质激素诱导的细胞凋亡。为此，我们提出假说：OCN/MiR-133a在VK对骨前体细胞"促分化、抗凋亡"中发挥重要作用，为VK预防激素型股骨头坏死奠定了基础。为验证此假说，我们设计了体外模拟乏氧的病理条件，采用RNAi,MiR-133a sponge技术等研究OCN/MiR-133a在"促分化、抗凋亡"中的作用。进而通过股骨头坏死动物模型的前瞻性预防实验，利用Micro-CT,免疫杂交技术等观察OCN/MiR-133a与股骨头坏死的预防结果。本研究通过OCN/MiR-133a途径，多层面研究VK预防激素型股骨头坏死的理论基础和结果。

In the background of corticosteroid-induced osteonecrosis of the femoral head (ONFH), the expression of osteogenic cytokine osteocalcin is downregulated. Vitamin K can regulate the carboxylation of osteocalcin, and MiR-133a plays an important role in the functionalization of osteocalcin. Our preliminary results showed that osteogenic differentiation of BMSC could be promoted in vitro by vitamin K treatment. Moreover, cellular apoptosis could be prevented in corticosteroid-induced ONFH. We hypothesize that osteocalcin/MiR-133a is critical for promoted differentiation and inhibited apoptosis when osteogenic precursor cells are treated by vitamin K. The promoted-differentiation and anti-apoptosis property of vitamin K is fundemental for the prevention of corticosteroid-induced ONFH. To verify our hypothesis, hypoxia will be used to mimic pathologic condition of ONFH. Methods of RNAi, MiR-133a sponge technique and so on are employed to reveal the role of osteocalcin/MiR-133a in promoted differentiation and inhibited apoptosis of vitamin K-treated osteogenic precursor cells in vitro. Furthermore, animal model of corticosteroid-induced ONFH will be designed for the investigation of preventive effects of vitamin K and osteocalcin/MiR-133a expression, through Micro-CT and in situ hybridization techniques.The current research can reveal the basic mechanism and the effect of vitamin K in the prevention of corticosteroid-induced ONFH in multiple aspects through the osteocalcin/MiR-133a pathway.