柚皮甙对大鼠心肌缺血再灌注损伤的保护作用

Protective effect of naringin on myocardial ischemia reperfusion injury in rats

目的探讨柚皮甙对心肌缺血再灌注损伤保护作用及机制。方法 50只雄性SD大鼠随机分为假手术组,缺血再灌注模型组,柚皮甙低,中,高剂量组。采用结扎冠状动脉左前降支,引起心肌缺血,放松丝线给予再灌注的方法建立心肌缺血再灌注损伤模型。柚皮甙低,中,高剂量组,于灌胃60 min后行缺血30 min,再灌注120 min,并监测其心律失常发生率。于再灌注结束后取心肌组织测定谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)和血清中肌酸激酶(CK)、乳酸脱氢酶(LDH)、过氧化氢酶(CAT)活性,心肌组织中丙二醛(MDA)含量,电镜观察心肌细胞超微结构。结果与模型组相比,柚皮甙三个不同剂量组大鼠心律失常发生率、血清中CK、LDH活性和心肌组织中MDA含量降低(P<0.05,P<0.01),血清中CAT、心肌组织中GSH-PX和SOD活性升高(P<0.01),心肌细胞超微结构损伤明显减轻。结论柚皮甙对缺血再灌注损伤心肌具有保护作用,与其抗氧化活性、减轻心肌细胞超微结构病理改变有关。

Objective To investigate the protective effect of naringin on myocardial ischemia repeffusion injury in rats and its possible mechanism. Methods Fifty SD rats were randomly divided into five groups： sham, model, low, middle and high dose of naringin groups. Left coronary artery braid, Silk suture tense and silk suture slacken were adopted to establish the model of myocardial ischemia reperfusion injury in anesthetized rats. 60 minutes after the last administration, the rats of naringin three doses groups were ligated for 30 minutes and reperfused for 120 minutes in the left anterior descending branch of coronary artery and detected the rate of arrhythmogenesis. At the end of reperfusion, the activities of glutathion peroxidase （GSH-Px） and superoxide dismutase （SOD） and the content of malondialdehyde （MDA） were detected in myocardial tissue, and the activities of creatine kinase （CK） , lactate dehydrogenase （LDH）, hydrogen peroxidase （CAT） in blood serum, and the ultra-structure of myocardial cells was observed with electron microscope. Results Compared with the model group, the three different dose groups of naringin decreased the rate of arrhythmogenesis and the activities of CK and LDH in blood serum and the content of MDA in myocardial tissue（P 〈0. 05 ,P 〈 0. 01 ）, and increased the activities of the CAT in blood serum and GSH-Px and SOD in myocardial tissue （P 〈 0. 01 ）, and obviously alleviated the injury of ultra-structure of myocardial cells. Conclusions Naringin has protective effects on myocardial ischemia reperfusion injury, which may be resulted from the activity of anti-oxidant and the change of pathology of alleviating ultra-structure of myocardial ceils.