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。

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 MTT, 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 signaling pathway may plays an important role in HGC impairing RGCs.