前期工作证实小间隙桥接法联合神经干细胞移植在改善周围神经功能方面具有肯定疗效，但是也暴露出细胞数量相对不足、轴突再生缓慢及突触功能缺陷等问题。新近研究发现，影响轴突再生及突触小泡释放的关键蛋白GAP-43和RIM1α均接受小类泛素修饰蛋白（SUMO）的精准调控，通过诱导SUMOs的时序性表达有望改善受损周围神经功能。本课题以条件性神经元特异性SUMO-1～3转基因小鼠的脊髓前角神经干细胞为供体，将其移植于部分脱乙酰甲壳质生物套管缝合的神经小桥接间隙，利用体外三维细胞培养模型和小鼠坐骨神经离断模型，通过Cre/loxP 重组系统和Tamoxifen介导调控的时序性表达机制，实现其在既定条件下的功能发挥，达到优化小间隙桥接法联合神经干细胞移植治疗周围神经损伤的目的。

Preliminary work demonstrated small gaps bridging combined with neural stem cell transplantation has showed a positive effect in terms of improving peripheral nerve function, but the problems also exposed,such as relatively insufficient of cells,slow axonal regeneration, synaptic dysfunction and other issues. Recent studies have found that GAP-43 and RIM1α underwent subcategories ubiquitin protein (SUMO) precision regulation , by inducing SUMOs timing of expression is expected to improve the damaged peripheral nerve function,and the GAP-43 is the key protein that affect axon regeneration and synaptic vesicle release. we use three-dimensional cell culture model and mouse sciatic nerve transection model, The SUMO modified neural stem cells derived from spinal cord is subject to the donor ,then transplant in small bridging gaps of peripheral axonal part chitosan biological conduit small nerve suture bridge the gap to play its function in the given conditions by Cre / loxP recombination system and Tamoxifen mediated sequential expression mechanism, to improve efficacy of neural stem cells combined with small gap sleeve bridging conduit system repair peripheral nerve injury.