牵张成骨是骨科肢体重建的常用技术，但治疗周期长和新骨形成缓慢是亟待解决的关键问题。中药骨碎补在骨伤科疾病中应用广泛，对促进骨折愈合疗效确切，特别是骨碎补的有效部位总黄酮作用显著。申请人前期研究发现，骨碎补总黄酮能够显著促进BMSCs成骨分化并诱导circRNA-MSR高表达。本课题提出骨碎补总黄酮通过circRNA-MSR介导的ceRNA机制调控Wnt信号通路促进成骨分化的设想。拟在体外构建BMSCs牵张模型观察骨碎补总黄酮对成骨分化的作用；利用慢病毒感染构建circRNA-MSR过表达的BMSCs，通过荧光素酶报告基因系统等分子生物学手段论证骨碎补总黄酮调控BMSCs成骨分化的分子机制；体内利用构建的兔股骨牵张成骨模型评估骨碎补总黄酮与circRNA-MSR通过激活Wnt信号通路促进牵张成骨的效果，进一步探讨骨碎补总黄酮促进牵张成骨的分子机制，并为中医药能够有效促进牵张成骨提供客观依据。

DO(Distraction osteogenesis) is a common technique for the reconstruction of limbs in orthopaedics,However,long treatment cycle and slow formation of new bone are the key problems to be solved urgently. Rhizoma Drynariae is widely used in orthopaedics diseases. It has a definite effect on promoting fracture healing, especially the total flavonoids in the effective part of Rhizoma Drynariae. The applicant's previous study found that total flavonoids from Rhizoma Drynariae（TFRD） can significantly promote osteogenic differentiation of BMSCs and induce high expression of circRNA-MSR. In this study, we propose that TFRD regulate Wnt signaling pathway to promote osteogenic differentiation through circRNA-MSR mediated ceRNA mechanism. In vitro we will establish distraction model of BMSCs to observe the effect of TFRD on osteogenic differentiation;and BMSCs overexpressed by circRNA-MSR were constructed by lentivirus infection，the molecular mechanism of TFRD in regulating osteogenic differentiation of BMSCs was demonstrated by molecular biological methods such as luciferase reporter gene system.In vivo DO model was established on the femur of rabbits to evaluate the effect of DO by Wnt signaling pathway that was activated of TFRD and circRNA-MSR,as well as further investigate the molecular mechanism of TFRD to promote distraction osteogenesis.