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大鼠视神经损伤的病理学和组织化学研究 被引量:1

Pathological and histochemical research of optic nerve injury in rats
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摘要 目的:拟通过对于视神经损伤后轴突的病理变化和GFAP及星形胶质细胞分泌的ECM阻抑性大分子CSPG的表达分布情况,观察视神经损伤后的修复反应,为进一步研究中枢神经纤维的再生提供实验资料。方法:首先建立大鼠视神经不完全损伤的挤压伤模型,于损伤后不同时间段取材进行HE染色和GFAP及CSPG的免疫组织化学研究。结果:HE染色示大鼠视神经损伤后3~7d小胶质细胞增殖吞噬功能活跃,伤后14d,损伤处可见多处新生血管。免疫组织化学结果示大鼠视神经损伤后7d,GFAP在损伤区缺乏表达,而CSPG在损伤区中心呈强阳性表达。结论:CNS轴突再生失败可能与损伤局部瘢痕形成的机械性阻碍和CSPG沉积的化学性阻碍有关。 AIM: To investigate the pathological changes of axon and the expression of ECM inhibiting chondroitin sulfate proteoglycan (CSPG) secrected by astrocytes after optic nerve injury, and to observe the repairing response of axon after injury so as to provide the experimental data for further research on regeneration of central nervous fiber. METHODS: Firstly, rat model was induced by means of incompletely crush wound of optic nerve using across action forceps behind eyeball. Then, we observed the injury of axon by HE and immunohistochemistry of GFAP and CSPG. RESULTS: HE indicated that microglial cells increased and its phagocytic function became active 3 to 7 days after injury. And neovascularization was observed after 14 days. The results of immunohistochemistry showed that the expression of GFAP was low at injured area, but CSPG presented a strong positive expression at the center of injured area 7 days after injury. CONCLUSION: The poor regeneration of optic nerve is partially related with neovascularization and CSPG deposit of injury site.
出处 《国际眼科杂志》 CAS 2008年第10期2015-2017,共3页 International Eye Science
基金 中国黑龙江省自然科学基金(No.D200517) 哈尔滨医科大学第二医院博士科研基金(No.BS2005-01)~~
关键词 视神经损伤 CSPG GFAP 免疫组化 optic nerve/crush wound chondroitin sulfate proteoglycan glial fibrillary acidic protein immuno-histochemistry
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