晶状体损伤促进视神经再生的作用及机制  

Effects of lens injury promotes optic nerve regeneration and related mechanisms

作　　者：潘凌[1] 郑华[1] 万瑾[1] 佘振珏[1] 肖虹蕾[1] 胡宝洋[1] 周国民[1] 

机构地区：[1]复旦大学上海医学院解剖与组织胚胎学系,上海200032

出　　处：《解剖学杂志》2006年第1期7-10,13,共5页Chinese Journal of Anatomy

基　　金：国家自然科学基金(30270699)教育部重大重点项目(102096)上海市曙光学者计划

摘　　要：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(LP),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.

关 键 词：视神经损伤 晶状体损伤 视神经 神经再生 巨噬细胞 

分 类 号：R770.2[医药卫生—眼科]