谷氨酰胺预处理上调热休克因子1活性影响热休克蛋白表达

Glutamine Preconditioning Induces Heat Shock Protein 70 Expression through the Regulation of Heat Shock Factor 1 on Ischemia/Reperfusion Insulted Rat Hearts

目的研究热休克因子1在谷氨酰胺诱导热休克蛋白表达中的作用。方法 30只SD大鼠随机分为三组:(1)对照组(C组,正常灌注90 min);(2)缺血再灌注组(I/R组,全心缺血30 min,复灌60 min);(3)谷氨酰胺组(G组,静脉注射谷氨酰胺0.75 g/kg,3小时后同I/R组行缺血再灌注处理)。记录各组冠脉流出液肌钙蛋白Ⅰ水平,测定复灌后心肌热休克蛋白70水平、热休克因子1蛋白表达水平及转录活性。结果与I/R组相比,G组肌钙蛋白Ⅰ水平降低(P<0.05),热休克蛋白70水平增高(P<0.05),热休克因子1蛋白表达未见显著影响(P>0.05),热休克因子1转录活性增高(P<0.05)。结论谷氨酰胺可减少缺血再灌注损伤大鼠的心肌酶释放水平,诱导热休克蛋白70表达,这一作用可能与其上调热休克因子1转录活性相关。

Objective The purpose of the study was to investigate the effects of heat shock factor 1 on glutamine-induced heat shock protein 70 expression. Methods Thirty SD rat hearts were harvested and randomly assigned to the following groups： the Control group （Group C, normal perfusion for 90 min）, the Ischemia/reperfusion group （Group I/R, global ischemia for 30 min followed by 60 min of reperfusion） and the Glutamine group （Group G, the rat received 0.75 g/kg glutamine intravenously, then the hearts were harvested and received ischemia! reperfusion protocol as group I/R described 3 hours later）. The cardiac troponin I levels, heat shock protein 70 levels, heat shock factor 1 levels and activities were measured. Results Compared with the I/R, group, the cardiac troponin I levels were decreased （P〈0.05）, while heat shock protein 70 levels and heat shock factor 1 activities were enhanced （P〈0.05）. There were no significant difference in heat shock factor 1 levels between the I/R and G groups. Conclusion Glutamine could induce heat shock protein 70 expression after ischemia/reperfusion injury; whcih might be related with the regulation of heat shock factor 1 activities.