目的:研究晶状体损伤对视神经再生的促进作用,并探讨巨噬细胞所起的作用。方法:成年SD大鼠钳夹造成视神经损伤模型(NC),戳伤晶状体(IP),玻璃体内注射酵母多糖(ZI)或注射体外活化的单核/巨噬细胞(MI),动物以此分组。用Nissl染色法显示存活的视网膜节细胞(RGCs),用抗GAP-43抗体标记轴突再生RGCs,用抗ED-1抗体标记活化的单核/巨噬细胞。结果:NC+LP组存活的RGCs比NC组明显增加,再生的RGCs及活化的单核/巨噬细胞都有明显增多的结果。NC+ZI组与NC+MI组也有类似结果。结论:晶状体损伤具有显著促进视神经再生的作用,其机制可能与趋化并激活巨噬细胞有关。
Objective: To study the neurite-promoting activity of lens injury on retinal ganglion cells (RGCs) and to explore the role of macrophages in this neuroprotection. Methods: Optic nerve injury was induced in adult SD rats by crushing the nerve (NC). Meanwhile, lens received intraocular penetration (LP); zymosan (ZI) or stimulated monocytes/macrophages (MI) were injected intravitrously. Animals were divided into 4 groups randomly. The survived RGCs were labeled by cresyl fast violet; the regenerating axons and RGCs were labeled by anti- GAP-43 antibody. Monocytes/macrophages were activated by anti-ED-1 antibody. Results: The number of survived RGCs in NC+LP group increased significantly. Increased GAP-43 expression and ED-1 positive cells were observed; similar results were obtained in NC+ZI group and NC+MI group. Conclusion: The findings indicate that lens injury has high neuroprotective and neurogenic activity, which may be related with the stimulation of macrophages.