神经干细胞移植对颈上交感神经节损毁兔MAP-2、GFAP表达的影响

The Effect of NSCs Transplantation on the Expression of MAP-2 and GFAP in Rabbits with Lesion of Superior Cervical Sympathetic Ganglion

目的研究神经干细胞(NSCs)移植对颈上交感神经节(SCSG)损毁兔胶质纤维酸性蛋白(GFAP)以及微管相关蛋白2(MAP2)表达的影响。方法 32只新西兰兔中8只为正常组不予处理,24只通过持针钳持续压榨兔SCSG10 s的方法构建SCSG损毁模型,均分成模型组、培养液组和干细胞组,造模后第7天分别给予等量的生理盐水、培养液及2×106个神经干细胞,移植后第1、7、10、14、21天分别记录各组兔损伤侧瞳孔直径变化,第21天取损伤侧SCSG进行HE染色,并进行免疫组化检测MAP-2和GFAP的表达。结果瞳孔直径变化情况,第10天、14天、21天干细胞组瞳孔直径均大于模型组和培养液组,差异有显著性(P<0.05);HE染色,干细胞组较模型组和培养液组细胞排列整齐,大小形态较一致,细胞间质增生少;免疫组化结果显示,干细胞可增加MAP-2的表达,降低GFAP的表达。结论神经干细胞通过促进兔损毁侧SCSG内MAP-2的表达,同时抑制GFAP的表达来发挥神经功能的修复作用。

Objective This study was to investigate the effects of Neural stem cells transplantation on the expression of MAP2 and GFAP for treatment in superior cervical sympathetic ganglion injury in rabbits. Methods 8 of the 32 New Zealand rabbits were recruited in normal group and no intervention was made,24 SCSG damage models were constructed by the method of continuous pressing of rabbit＇s SCSG for 10 seconds ,which were divided into model group, culture-medium group and stem cells group,the same amount of normal saline,culture media and 2 × 106 neural stem cells were given seven days after modeling.The changes of pupil diameter in four groups were observed and recorded 1,7,10,14,21 days after transplantation. HE staining was performed and the expression of MAP-2 and GFAP were detected by immunohistochemistry on the twenty-first day. Results The changes of pupil diameter in injured side of rabbits in stem cells group, compared with model group and culture-medium group,were statistically significant on days of 10,14, and 21 （P〈0.05）.Compared with model group and culture-medium group, cells in the stem ceils group were arranged in order,size and shape were uniform,and have a small amount of interstitial cell hy- perplasia.Immunohistochemistry results showed that stem ceils could increase the expression of MAP-2 and decrease the expression of GFAP. Conclusion Neural stem ceils transplantation is able to repair the nerve function of the damaged SCSG in rabbits, and its mechanism may be related to promoting the expression of MAP-2 and inhibiting the expression of GFAP.