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目的:探讨Nogo受体(NgR)在糖尿病视网膜病变中的作用及下游分子机制。方法:雄性SD大鼠腹腔注射链脲佐菌素诱导糖尿病模型,糖尿病大鼠玻璃体腔内注射病毒包装的NgR反义核苷酸序列(siNgR组)、阴性核苷酸序列(scRNA对照组)或空白病毒液(糖尿病组),玻璃体腔内注射空白病毒液的正常SD大鼠为正常对照组。3个月视网膜HE染色,观察视网膜神经层厚度及节细胞密度的变化,免疫荧光组化检测NgR及其下游分子N-甲基-D-天门冬氨酸2B受体(NR2B)在视网膜神经节细胞内的共存情况,Western Blot检测NgR及NR2B在视网膜内的表达。结果:与正常对照组相比糖尿病组及scRNA对照组视网膜明显变薄、神经节细胞密度降低,siNgR组无明显变化。NgR与NR2B均表达于视网膜节细胞层,二者在视网膜神经节细胞内大量共存。与正常对照组相比,糖尿病组、scRNA对照组视网膜NgR及NR2B表达均明显增加(P<0.01),而siNgR组NgR及NR2B表达均无明显变化。结论:NgR/NR2B信号通路激活可能是糖尿病大鼠RGC数量减少的重要原因之一。
Objective: To investigate the role of Nogo receptor (NgR) in diabetic retinopathy and its downstream molecular mechanisms. Methods: Male Sprague-Dawley rats were injected intraperitoneally with streptozotocin-induced diabetic model. The NgR antisense nucleotide sequence (siNgR group), negative nucleotide sequence (scRNA control group) or The blank virus solution (diabetic group) and the normal SD rats injected with empty virus solution into the vitreous cavity were normal control group. Retinal HE staining was performed at 3 months to observe the changes of retinal nerve layer thickness and ganglion cell density. Immunofluorescence staining was used to detect the expression of NgR and its downstream molecule N-methyl-D-aspartate 2B receptor (NR2B) Intracellular coexistence, Western Blot detection of NgR and NR2B expression in the retina. Results: Compared with the normal control group, the retina of the diabetic group and the scRNA control group were significantly thinner, the ganglion cell density was decreased, and there was no significant change in the siNgR group. NgR and NR2B were expressed in the retinal ganglion cell layer, both in retinal ganglion cells coexist in large numbers. Compared with normal control group, the expression of NgR and NR2B in diabetic group and scRNA control group were significantly increased (P <0.01), while the expression of NgR and NR2B in siNgR group had no significant change. Conclusion: The activation of NgR / NR2B signaling pathway may be one of the important reasons for the decrease of RGCs in diabetic rats.