中文摘要：

目的探讨缺血后处理对短暂脑缺血后海马CA1区神经元内蛋白伴侣的影响。方法采用大鼠全脑缺血模型。Wistar大鼠分为缺血组及缺血后处理组,每组按照再灌注时间进一步分为12 h恢复组、24 h恢复组、48 h恢复组及72 h恢复组。采用HE染色光镜观察脑缺血后神经元死亡;差速离心结合蛋白印迹分析短暂脑缺血后蛋白伴侣hsp70和hsp40在细胞内数量的变化。结果 HE染色显示缺血后处理显著降低了脑缺血再灌注后海马CA1区神经元死亡;蛋白印迹分析显示,缺血后处理显著提高了hsp70的表达,同时还降低了缺血再灌注所致的hsp40的减少。结论缺血后处理能够显著减少脑缺血后海马CA1区神经元内hsp70和hsp40的含量,进而抑制蛋白聚集物的形成,降低了缺血再灌注后海马CA1区神经元死亡。

英文摘要：

Objective To investigate the effects of ischemic postconditioning on the chaperones in the CA1 neurons suffered transient ischemia and reperfusion.Methods Transient global ischemia rat model was established.Following different reperfusion period,all the Wistar rats were divided into ischemia and ischemic postconditioning groups.Each group was divided further into sham-operation,12,24,48 and 72 h recovery groups.Differential centrifuge and Western blotting analysis were used to analyze the quantitative alterations of hsp40 and hsp70.Results HE staining showed that ischemic postconditioning reduced neuronal death induced by transient ischemia and reperfusion.Western blotting analysis showed that the expression of hsp70 was upregulated,and the content of hsp40 in CA1 neurons was improved by ischemic postconditioning.Conclusions Ischemic postconditioning could improve the quantities of hsp70 and hsp40 in the CA1 neurons,and reduce neuronal death in the CA1 region caused by ischemia and reperfusion.