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大鼠颈部止血带诱导脑缺血后脑神经元变性及热休克蛋白(72)表达的时间进程。

Time course of brain neuronal degeneration and heat shock protein (72) expression following neck tourniquet-induced cerebral ischemia in the rat.

作者信息

Cizkova D, Vanicky I, Ishikawa T, Marsala M

机构信息

Institute of Neurobiology, SAS, Kosice, Slovak Republic.

出版信息

Cell Mol Neurobiol. 2000 Jun;20(3):367-81. doi: 10.1023/a:1007018327133.

Abstract
  1. The present study was designed to examine the regional expression of HSP72/73 protein after a 7.5-min period of cerebral ischemia and to compare the distribution of HSP neurons with the localization of irreversible neuronal degeneration as analyzed by silver impregnation technique. 2. During 6-24 hr after cerebral ischemia clear-cut neuronal argyrophilia developed in several brain regions including the hippocampal hilus, nucleus reticularis thalami, and colliculi inferiores. With the exception of the hippocampal hilus, the structures which showed silver impregnability were HSP72 negative at 6-24 hr. 3. Despite the clear HSP72 expression seen in hippocampal CA1 neurons, a significant loss of these neurons was seen at 7 days after ischemia. 4. These data show that in some structures the presence of HSP72 is indicative of higher resistance of these neurons to ischemia-induced degeneration, however, the process of delayed neuronal degeneration appears to be independent of the accelerated synthesis of HSP72 seen during the early period of reflow.
摘要
  1. 本研究旨在检测脑缺血7.5分钟后HSP72/73蛋白的区域表达情况,并通过银浸染技术分析,比较HSP神经元的分布与不可逆神经元变性的定位。2. 脑缺血后6至24小时内,包括海马齿状回、丘脑网状核和下丘等几个脑区出现明显的神经元嗜银性。除海马齿状回外,在6至24小时显示银浸染性的结构HSP72呈阴性。3. 尽管在海马CA1神经元中可见明显的HSP72表达,但缺血7天后这些神经元出现明显丢失。4. 这些数据表明,在某些结构中,HSP72的存在表明这些神经元对缺血诱导的变性具有更高的抵抗力,然而,延迟性神经元变性过程似乎与再灌注早期所见的HSP72加速合成无关。

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