热耐受减低鼠脑海马CA_1区缺血后hsp70mRNA的诱导

Reduction of hsp 70 mRNA after Ischemia and Reperfusion in CA1 Sector of Hippocampus in Low Thermotolerance Rats

目的:观察海马缺血再灌注后hsp70mRNA的诱导,及其在迟发神经元死亡(DND)的作用意义。方法:制备热耐受及大鼠前脑缺血模型。观察海马CA1区锥体细胞存活情况,并用原位杂交技术检测hsp70mRNA的诱导情况。结果:短暂缺血后海马CA1区出现DND。热耐受后缺血组的神经元损害明显减轻,hap70mRNA表达与缺血组相比明显减低。结论:hsp70表达增强是减少DND的机制之一,而hap70mRNA可能是应激状态较好的指标。将2者综合分析,可以更有效地评价细胞损伤程度与疗效。

Objective: To clarify the reduction of hsp70 mRNA after ischemia and reperfusion in CA1 sector of hippocampus in low thermotolerance rats and its role on delayed neuronal death (DND). Methods: Thermotolerance'and forebrain ischemic rat models were produced. The number of normal neurons in CAt sector was assessed. The reduction of hsp70 mRNA was detected with the method of in situ hybridization. Results: DND occurred in CAj sector of hippocampus after trasient ischemia. The neuronal damage was obviously abated after thermotolerance in the ischemic group. The expression of hsp70 mRNA in the thermotolerance group was signifiantly lower than in the ischemic group. Conclusion: The enhanced hsp70 irnmunoactivity might be one of the mechanisms for preventing cells from DND, hsp70 mRNA provides a sensitive index of stress response. The combined evaluation of hsp70 gene and protein levels will provide a more practical and precise marker for cell damages and therapeutic approaches.