Faslg在大鼠坐骨神经损伤修复与再生过程中的作用机制研究

神经损伤修复与功能重建依然是当今神经科学研究的前沿和热点。周围神经损伤后随即发生Wallerian溃变，在此过程中大量基因的表达变化为损伤神经的修复与再生创造了有利条件，然而，Wallerian溃变引起的基因表达促进损伤神经修复与再生的可能机制仍不明确。本项目中，我们采用生物信息学和分子生物学技术，研究大鼠坐骨神经Wallerian溃变过程中Faslg (Fas ligand gene) 的表达变化以及其调控神经损伤修复与再生的分子机制。初步研究显示：Faslg的体内外表达变化影响了施万细胞的增殖、迁移和凋亡以及相关因子的表达，且Faslg可能通过p-ERK/ERK、p-AKT/AKT和NF-κB等信号转导途径调控大鼠损伤神经的修复与再生。该项目的深入开展可望从分子水平揭示Faslg在周围神经损伤修复与再生过程中的作用机制，为周围神经损伤修复与功能重建等临床相关研究提供实验基础和理论依据。

Nerve injury and repair is still an important area of research in modern neuroscience. Wallerian degeneration (WD) happened immediately following peripheral nerve injury. A large number of genes are differentially regulated during the process of WD, which is of great importance for nerve repair and regeneration, but the precise mechanisms responsible for these gene expressions during WD are not completely understood. Here, by using bioinformatics and molecular biology analysis, we investigated the expression of Faslg (Fas ligand gene) in the distal nerve stump, explored the molecular mechanisms of Faslg affected sciatic nerve repair and regeneration during WD after rat sciatic nerve injury. Recently, we found that the expression changes of Faslg affected Schwann cell (SC) migration, proliferation, apoptosis, and relative factors release in vitro and vivo. Furthermore we found that Faslg may regulated nerve repair and regeneration by p-ERK/ERK, p-AKT/AKT, and NF-κB signal pathways during WD after rat nerve injury. The study will provide us with a firmer basis on the molecular mechanisms of Faslg regulating nerve degeneration and/or regeneration in nerve injury and repair.