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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 To investigate the role of heat shock factor 1 in glutamine-induced heat shock protein expression. Methods Thirty SD rats were randomly divided into three groups: (1) control group (C group, normal perfusion 90 min); (2) ischemia / reperfusion group (I / R group, 60 min); (3) glutamine group (G group, intravenous injection of glutamine 0.75 g / kg, 3 hours later, with I / R group ischemia reperfusion treatment). The levels of cardiac troponin I in coronary effusion were recorded and the level of heat shock protein 70, heat shock factor 1 protein and transcriptional activity were measured after reperfusion. Results Compared with the I / R group, the levels of Troponin I (P <0.05), heat shock protein 70 (P <0.05) and heat shock factor 1 (P> 0.05) , Heat shock factor 1 transcriptional activity increased (P <0.05). Conclusion Glutamine can reduce the level of myocardial enzyme release and induce the expression of heat shock protein 70 in rats with ischemia-reperfusion injury, which may be related to its upregulation of the transcriptional activity of heat shock factor 1.