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晶状体损伤促进视神经再生的作用及机制
  • ISSN号:1001-1633
  • 期刊名称:《解剖学杂志》
  • 时间:0
  • 分类:R774.6[医药卫生—眼科;医药卫生—临床医学] R776.1[医药卫生—眼科;医药卫生—临床医学]
  • 作者机构:[1]复旦大学上海医学院解剖与组织胚胎学系,上海200032
  • 相关基金: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
中文摘要:

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(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。

英文摘要:

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.

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期刊信息
  • 《解剖学杂志》
  • 北大核心期刊(2011版)
  • 主管单位:中国科学技术协会
  • 主办单位:中国解剖学会
  • 主编:张传森
  • 地址:上海市翔殷路800号
  • 邮编:200433
  • 邮箱:jpxzz01@126.com
  • 电话:021-81870955
  • 国际标准刊号:ISSN:1001-1633
  • 国内统一刊号:ISSN:31-1285/R
  • 邮发代号:4-380
  • 获奖情况:
  • 国内外数据库收录:
  • 美国化学文摘(网络版),日本日本科学技术振兴机构数据库,中国中国科技核心期刊,中国北大核心期刊(2004版),中国北大核心期刊(2008版),中国北大核心期刊(2011版),中国北大核心期刊(2014版),中国北大核心期刊(2000版)
  • 被引量:12391