摘要
目的:观察尿激酶溶栓治疗对神经细胞骨架结构微管相关蛋白-2(MAP-2)的影响。方法:用自体血栓法制 作大鼠大脑中动脉闭塞(MCAO)模型,在MCAO后30min静脉注射尿激酶(UK)溶栓,通过神经功能评分判断溶栓的疗 效,HE染色进行病理观察,用免疫组织化学的方法研究溶栓对缺血皮层和海马MAP-2蛋白表达的影响。结果:溶栓组 神经功能评分较未溶栓组有显著提高,HE染色见病变范围明显缩小。MCAO后2h缺血区树突MAP-2表达较对照组 即有明显下降(P<0．05),随着缺血时间延长树突及胞体MAP-2降解增加,而溶栓治疗各时间点MAP-2表达较未溶栓 组显著提高(P<0．01)。结论:减少MAP-2的降解可能是溶栓治疗改善神经功能的机制之一。溶栓治疗后早期半暗带 区MAP-2表达在树突减少而在神经元胞体基本正常,这可能是缺血后神经元顿抑的形态学基础。
Objective： To observe the effects of tbrombolysis therapy on microtubule-associated protein 2 （MAP-2） in rat with acute cerebral infarction. Methods： The middle cerebral artery occlusion （MCAO） model was induced in rats by autologous clot. Urokinase （UK, 5 P% u/kg） was injected intravenous at 30 minutes after MCAO . The efficacy of UK was evaluated by neurologic deficit score, histological features were identified by hematoxylin and eosin （HE） staining, The immunohistochemistry technique was used to evaluate the effect of thrombolysis therapy on expression of MAP2 protein in rat with cerebral infarction. Results： The neurologic deficit score was significantly improved by injection of UK. The ischemic lesion in UK groups was slighter than in MCAO alone groups. At 2 hours after MCAO the express of MAP-2 in dendrites decreased significantly. With the time of cerebral ischemia density of MAP-2 was decreased in dendrites and soma of neuron. In all thrombolysis therapy groups the expression MA.P-2 is higher than that in MCAO groups at same time point, Conclusion： Preventing degradation of MAP2 induced by cerebral ischemia may be one of the mechanisms that thrombolysis therapy can improve neurologic function. Expression of MAP-2 decreased in dendrite and it was nearly no change in soma of neuron of penumbra, maybe this is the morphological foundation of Neuron Stunning.
出处
《脑与神经疾病杂志》
2005年第6期446-449,共4页
Journal of Brain and Nervous Diseases
基金
湖北省科技攻关项目资助(No 2003AA301C50)
关键词
大鼠
脑梗死
溶栓治疗
微管相关蛋白2
神经元顿抑
Rat cerebral infarction thrombolysis microtubule-associated protein 2 Neuron Stunning
