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目的 探讨葛根素对缺血再灌注损伤心肌的保护及其作用机制。方法 ( 1)采用TTC染色测定入选各组患者心肌梗死的范围 ,并在电镜下对缺血区心肌进行超微结构观察。 ( 2 )采用放免法、免疫组化法检测血清超氧化物岐化酶 (SOD)、血浆内皮素 (ET)的浓度和心肌组织BCL 2蛋白的表达情况。结果 葛根素组与 0 .9%氯化钠组比较 ,葛根素可明显减小心肌梗死范围 (P <0 .0 1) ,改善其超微结构的变化 ;葛根素能增加血清SOD的活性、降低血浆ET浓度 (P <0 .0 5 ) ;葛根素组与假手术、0 .9%氯化钠组比较 ,葛根素能显著上调缺血再灌注心肌BCL 2蛋白的表达 (P <0 .0 0 1)。结论 葛根素可明显减轻心肌缺血再灌注损伤 ,其心肌保护机制可能是通过其增加血清SOD的活性、降低血浆ET的浓度并促进缺血再灌注心肌BCL 2蛋白的表达来实现的
Objective To investigate the protective effect of puerarin on myocardial ischemia-reperfusion injury and its mechanism. Methods (1) TTC staining was used to determine the range of myocardial infarction in each group. The ultrastructure of ischemic myocardium was observed under electron microscope. (2) The serum levels of superoxide dismutase (SOD), plasma endothelin (ET) and the expression of BCL 2 protein in myocardium were detected by radioimmunoassay and immunohistochemistry. Results Compared with 0.9% sodium chloride group, puerarin significantly decreased the infarct size (P <0.01) and improved the ultrastructural changes of puerarin. Puerarin could increase the activity of SOD, (P <0.05). Compared with sham-operated group and 0.9% sodium chloride group, puerarin significantly up-regulated the expression of BCL-2 in myocardium after ischemia-reperfusion (P <0.05) 0 0 1). Conclusion Puerarin can significantly reduce myocardial ischemia-reperfusion injury, and its myocardial protection mechanism may be through its activity of increasing serum SOD, reducing plasma ET concentration and promoting myocardial ischemia-reperfusion BCL 2 protein expression to achieve