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葛根素对心肌缺血再灌注损伤保护作用的实验研究 被引量:15

Experimental study of the myocardial protection of puerarin on the model of myocardial ischemia-reperfusion injury in Rabbits
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摘要 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 Objective To investigate the effect of myocardial protection of puerarin on myocardial ischemia reperfusion injury in rabbits and its mechanism.Methods (1)Infarcted sizes in myocardial were estimated by dye method and the myocardial ultrastructure at the ischemia region was observed under the electron miscroscope.(2)The serum concentrations of superoxide dismutase(SOD)、plasma edothelin (ET) and the expression of bcl-2 protein in rabbits in groups pretreated by puerarin (50mg/kg,iv) were measured by radioimmunoassay and immunohistochemistry.Results Compared with the 0.9% sodium chloride groups, the infarcted size were significantly decreased (P<0.01) and the damage of the myocardial ultrastrueture was significantly ameliorated in the puerarin-treated group;Puerarin can increase the serum concentrations of SOD and decrease the plasma concentrations of ET significantly (P<0.05);Compared with the control group and 0.9% sodium chloride group,puerarin can significantly increased the expression of bcl-2 protein in ischemia reperfusion myocardial (P<0.001).Conclusion Puerarin can reduce myocardial ischemia reperfusion injury significantly.The myocardial protection of puerarin may be realized by increasing the serum concentrations of SOD、reducing the plasma concentrations of ET and increasing the expression of bcl-2 protein.
出处 《临床内科杂志》 CAS 北大核心 2004年第11期779-781,共3页 Journal of Clinical Internal Medicine
关键词 葛根素 心肌缺血再灌注损伤 血清超氧化物岐化酶 血浆内皮素 BCL-2蛋白 Puerarin Myocardial Ischemia Reperfusion Injury SOD ET B cl-2
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