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作 者:王建国[1] 陈群[1] 曾因明[1] 李德馨[2]
机构地区:[1]徐州医学院江苏省麻醉学重点实验室,徐州市221002 [2]南京军区总医院
出 处:《临床麻醉学杂志》2001年第4期206-208,共3页Journal of Clinical Anesthesiology
基 金:江苏省青年科技基金! (No .BQ980 0 9);江苏省麻醉学重点实验室开放课题基金! (No .K9844)
摘 要:目的 研究脑缺血再灌注期间海马CA1区锥体细胞微管运动蛋白kinesin活性的变化与延迟性神经元死亡 (delayedneurondeath ,DND)的关系。 方法 沙土鼠前脑缺血再灌注模型 ,脑缺血时间为 10分钟。采用免疫组织化学方法结合计算机图象分析技术测定kinesin的免疫活性。组织学检查判断DND。结果 脑缺血再灌注后海马CA1区微管运动蛋白kinesin的活性明显下降 ,在再灌注 6、48和 96小时其活性分别仅为假手术组的 49%、32 %和 12 % (P <0 0 1)。在再灌注 96小时 ,CA1区出现明显的DND ,而CA2、CA3、CA4微管运动蛋白活性无明显变化。结论 脑缺血再灌注后海马CA1区微管运动蛋白活性进行性下降 。Objective To explore the relationship between the change of activity microtubule based motor(kinesin) and delayed neuron death.Methods The cerebral ischemia models of gerbils were achieved by occlusing bilateral carotid arteries.The activity of kinesin in the hippocampus was determined by using immunohistochemical staining and computer image analysis system.Delayed neurons death was assayed by histological examination.Results The activity of kinesin in the hippocampus CA1 sector significantly decreased after reperfusion and its activities at 6h、48h and 96h reperfusion were about 49%、32% and 12% of that in sham-operated group respectively.However,the activity of kinesin in the hippocampus CA2、CA3 and CA4 sector during cerebral ischemia/reperfusion was ot reduced significantly.Conclusion Cerebral ischemia/reperfusion causes delayed neurons death,which may be the result of the decrease in the kinesin activity.
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