葡萄糖酸锌对心肌缺血/再灌注损伤保护作用的动物实验研究

目的 探讨葡萄糖酸锌(ZG)对心肌缺血/再灌注损伤保护作用及其机制.方法 将50只雄性SD大鼠随机分为5组,即假手术组,模型组,ZG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.ZG低、中、高剂量组,于末次灌胃1 h后行缺血30 min,再灌注60 min.于再灌注结束后取心肌组织测定钠-钾-三磷酸腺苷酶(Na+-K+-ATPase)、超氧化物歧化酶(SOD)活性、IL-1β、Ca2+和丙二醛(MDA)含量.结果 与模型组相比,ZG 3个剂量组大鼠心肌组织中Na+-K+-ATPase和SOD活性升高,IL-1β、Ca2+

Animal experiment on cardioprotective effects of zinc gluconate on myocardial ischemia/reperfusion injury

Objective To investigate the protective effect of zinc gluconate on myocardial ischemia/reperfusion injury in rats and its possible mechanism.Methods Fifty SD rats were randomly divided into five groups:sham,model,ZG of low,middle and high dose 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.At 1 h after the last administration,the rats of ZG three groups were ligated for 30 min and reperfused for 60 min in the left anterior descending branch of coronary artery.Myocardial tissue was collected at the end of reperfusion for detecting the activitise of Na+-K+-ATPase and SOD,the contents of IL-1β,Ca2+ and MDA.Results Compared with the model group,the three different dose groups of ZG increased the activitise of Na+-K+-ATPase and SOD,decreased the contents of IL-1β,Ca2+ and MDA.Conclusion ZG has protective effects on myocardial ischemia/reperfusion injury.The mechanism is the inhibition of hydroxyl radical(·OH) generation,the reduction of lipid peroxidation,the improvement of cardiac energy metabolism,the reduction of calcium overload and the inhibition of inflammatory response.