中文摘要：

目的：探讨NgR-Rock信号通路在高浓度葡萄糖损伤视网膜神经节细胞（retinal ganglion cells,RGCs）中的机制。方法：实验分4组：对照组、高糖组、SiNgR组（高糖培养基中加入AAV2-siNgR病毒）和SiRNA空白组（高糖培养基中加入阴性核甘酸序列）。在培养的第3d观察细胞生长状态;Western blot检测NgR、Rock及F-actin的表达;MTT法检测细胞活力;利用F-actin免疫组织化学染色显示细胞形态。结果：与对照组相比,高糖组及SiRNA空白组细胞体积缩小,突起较少,细胞折光性增强;NgR及Rock的表达明显上调,F-actin表达减少,细胞活力下降（P〈0.05）;而SiNgR组与对照组相比NgR、Rock及F-actin的表达,细胞活力无明显改变（P〉0.05）。结论：NgR-Rock信号通路激活可能是导致高糖环境中RGC损伤的重要机制之一。

英文摘要：

AIM： To investigate the role of NgR-Rock signaling pathway in the retinal ganglion cells （RGCs） which are damaged by high concentration of glucose. METHODS： Studies were performed with control group, high glucose concentration （HGC） group, SiNgR group （HGC medium including AAV2-SiNgR virus） and SiRNA control group （HGC medium including the negative sequence of nucleotides）. Three days after culture, RGCs was observed by microscope, expressions of NgR, Rock and F-actin were detected by Western blot, cell vitality was determined by M＇l-I-, and cell morphology was also detected by F-actin immunohistochemical staining. RESULTS. Compared with control group, in HGC and control SiRNA groups, cell volume decreased with less processes, light refraction was strengthened, and the expressions of Rock and NgR were significantly increased （P〈0.05 , respectively）, while the expression of F-actin was reduced （ P〈 0.05） ; Compared with control group, there was no obvious difference in the expression of NgR, Rock and F-actin, and cell vitality between SiNgR group and control group （P〉0.05）. CONCLUSION= The activation of NgR-Rock signalingpathway may plays an important role in HGC impairing RGCs.