阳离子脂质体转染神经营养因子3基因修饰许旺细胞与基质凝胶桥接损伤的坐骨神经

背景：周围神经损伤后给予外源性神经营养因子3对促进神经再生及保护肌萎缩均有作用。目的：观察阳离子脂质体转染神经营养因子3基因修饰的许旺细胞与细胞外基质凝胶桥接修复坐骨神经损伤的效果。方法：取80只成年Wistar大鼠制作左侧坐骨神经缺损模型,随机分组,以不同材料进行修复：细胞外基质凝胶组、许旺细胞-聚乳酸/羟基乙酸共聚物-细胞外基质凝胶组、神经营养因子3基因-聚乳酸/羟基乙酸共聚物-细胞外基质凝胶组、神经营养因子3基因修饰许旺细胞-聚乳酸/羟基乙酸共聚物-细胞外基质凝胶组。结果与结论：①腓肠肌肌肉组织学检查：术后8,12周神经营养因子3基因修饰许旺细胞-聚乳酸/聚羟基乙酸共聚物-细胞外基质凝胶组腓肠肌横截面积结构清晰、肌纤维粗大,呈基本正常肌肉结构,纤维组织较少,肌横截面积明显大于其他3组（P〈0.05,P〈0.01）。②肌细胞凋亡检测：术后4,8,12周神经营养因子3基因修饰许旺细胞-聚乳酸/聚羟基乙酸共聚物-细胞外基质凝胶组肌细胞凋亡数低于其他3组（P〈0.05）。表明阳离子脂质体转染神经营养因子3基因修饰的许旺细胞与细胞外基质凝胶可较好修复损伤神经,防止失神经肌萎缩细胞凋亡。

Effect of neurotrophic factor 3 modified Schwann cells via cationic liposome transfection on nerve defects induced by sol-gel bridging

BACKGROUND： After peripheral nerve injury, exogenous neurotrophic factor 3 （NT-3） can promote neural regeneration and protect muscle atrophy. OBJECTIVE： To observe the effects of NT-3 modified Schwann cells via cationic liposome transfection on repairing nerve defects induced by sol-gel bridging. METHODS： Eighty adult Wistar rats were used to prepare left sciatic nerve defect models and then randomly divided into four groups： extracellular matrix gel group （A）, Schwann cells-poly lactic acid/glycolic acid-extracellular matrix gel group （B）, NT-3-polylactic acid/giycolic acid-extracellular matrix gel group （C）, NT-3 modified Schwann cells-polylactic acid/glycolic acid-extracellular matrix gel group （D）. RESULTS AND CONCLUSION：① Histological examination of gastrocnemius muscle： Gastrocnemius in group D had a clear structure based on the cross-sectional area, thick muscle fibers were thick, and presented with an essentially normal muscle structure as well as there were fewer fibrous tissues. The cross-sectional muscle area in group D was significantly greater than that in the other three groups （P 〈 0.05, P 〈 0.01）. ②Myocyte apoptosis detection： The number of apoptotic cells in group D was lower than that in the other three groups （P 〈 0.05）. These findings demonstrate that NT-3 genes modified Schwann cells by cationic liposomes transfection and extracellular matrix gel can efficiently repair nerve injury and prevent myocyte apoptosis following denervated muscle atrophy.