热休克蛋白70在鼠脑缺血/再灌注损伤的表达

The expression of the heat shock protein70 in the cerebral ischemic reperfusion injury in rats

目的:为了加深了解热休克蛋白70(HSP70)与脑缺血/再灌注损伤的关系,探讨HSP70的表达与细胞形态学变化。方法:24只SD大鼠通过左颈总动脉灌注生理盐水形成轻度左侧脑缺血。其中12只大鼠为单纯缺血组,另12只为缺血30分钟后再灌注30分钟组。两组切片分别进行免疫细胞化学和病理组织学观察。结果:我们发现脑缺血30分钟HSP70在顶叶皮层表达,分布在细胞膜,轴突和树突中。再灌注30分钟无HSP70表达。结论:局灶性脑缺血可诱导HSP70表达,恢复血循环无HSP70表达。

Objective:To enhance our understanding of the relation between cerebral ischemic rperfusion injury and heat shock protein70 (HSP70) expression. We evaluated the cellular expression of HSP70 in conjunction with the morphological analysis of rat brain. Methods: Twenty -four Sprague-Dawley (SD) rats were subjected to mild brain ischemia by infusion normal saline 30 minutes from the left common carotid artery. Twelve to them were cerebrel ischemia 30 minutes. The other twelve rats were studied after brain ischemia 30 minutes and reperfused for 30 minutes by collateral circulation. Brain sections were analyzed by immunohistochemical staining (using a monoclonal antibody to HSP70) and pathological staining (hematoxylin and eosin staining,HE). Results: We found that HSP70 was firstly expressed in parietal cortices when cerebral ischemia 30 minutes. The HSP70 expressed in neuron's membrane, axon and dendrite. Afer brain ischemia 30 minutes and reperfussion 30 minutes by collateral circulation, we can not observe HSP70 in neurons. These results are not the same as reported before. Conclusion: Focal cerebral ischemia could induce the HSP70 in injured cells. If circulation recovery, no HSP70 can be found.