椎板切除术后硬膜外瘢痕粘连是影响临床疗效的重要原因之一。我们发现他克莫司能通过诱导成纤维细胞凋亡预防硬膜外瘢痕粘连，基因芯片结果显示miR-429低表达于他克莫司刺激后的人成纤维细胞。前期研究发现抑制miR-429功能可以增加药物诱导成纤维细胞的凋亡率，生物信息学分析及荧光素酶报告基因系统验证结果发现并证实RhoE是miR-429的靶基因。RhoE是PI3K信号通道的重要抑制因子，可通过抑制细胞周期诱导细胞凋亡。本课题拟以miR-429为切入点，采用Western-Blot、qRT-PCR、慢病毒转染、动物体内实验等方法，从体内、体外研究阐述miR-429 调控RhoE/PI3K通道诱导成纤维细胞凋亡减少硬膜外瘢痕粘连的确切机制。本研究有助于明确miR-429在人成纤维细胞凋亡中的作用及其预防硬膜外瘢痕粘连的分子学机制，为硬膜外瘢痕粘连的防治防治提供新思路及潜在治疗靶点。

Epidural scar adhesion after laminectomy is one of the important factors affecting the clinical curative effect. We found that the tacrolimus-induced apoptosis in fibroblast can prevent epidural scar adhesion. Gene chip technology showed that miR-429 is in low expression in fibroblasts after stimulated of tacrolimus. Previous studies have suggested that inhibiting the function of miR-429 can increase the rate of drug-induced apoptosis of fibroblast, bioinformatics analysis and luciferase reporter gene system verification results found and confirmed RhoE is the target genes of miR-429. RhoE is an important inhibitory factor of PI3K signaling pathway, which can induce apoptosis by inhibiting the cell cycle. This study picks miR-429 molecules as the breakthrough point, and it will use Western-Blot, qRT-PCR, Lentiviral Infection, animal models and so on to clarify the exact molecular mechanisms of miR-429-induced fibroblast apoptosis by RhoE/PI3K pathway. This study helps to clear miR-429 in the role of fibroblast apoptosis and the molecular mechanisms of the prevention of epidural scar adhesion. Also, it provides new ideas and potential therapeutic target to prevent and cure epidural scar adhesion.