摘要
目的观察地奥心血康(DK)对大鼠心肌缺血再灌注损伤的影响。方法48只W istar大白鼠随机分为正常对照组、模型对照组与DK组。前2组每日灌胃0.5%CMC 10mL/kg,DK组每日灌胃DK 70mg/kg,共10天。末次给药后24h结扎大鼠冠状动脉左前降支30m in,再灌注90m in复制大鼠心肌缺血再灌注损伤模型,观察心律失常评分、心肌梗死面积、心功能、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、心肌Na+-K+-ATP酶和Ca2+-ATP酶活性及丙二醛(MDA)含量等的变化。结果与模型对照组相比,DK组心律失常评分明显降低,心肌梗死面积明显缩小,心功能明显改善,SOD、CAT及GSH-Px、Na+-K+-ATP酶、Ca2+-ATP酶活性显著升高、MDA含量显著降低。结论DK对大鼠心肌缺血再灌注损伤有保护作用。其机制可能与清除自由基,抑制脂质过氧化有关。
OBJECTIVE To observe the effects of DK on myocardial ischemia reperfusion injury in rats. METHODS 48 Wistar rats were randomly divided into three groups : normal control group, model control group and DK treatment group. Those of the former two groups were treated with gastrogavage of 0.5% CMC 10mL/kg · d for 10 days, and the treatment group with DK 70mg/kg · d. Myocardial ischemia reperfusion injury models were established by the ligation of left desending coronary artery for 30min and reperfusion for 90min in rats and the influence on scores of arrhythmia, myocardial infarction size, cardiac function, the activities of superoxide dismutase ( SOD), catalase (CAT) , glutathione peroxidase ( GSH-Px), Na^+ -K^+ -ATPase, Ca^2+ -ATPase, and the content of malondialdehyde(MDA) were determined. RESULTS In DK-treatment group, the score of arrhythmia decreased, the myocardial infarction size diminished, the cardiac function was markedly improved, the activities of SOD, CAT, GSH-Px, Na^+ -K^+ -ATPase and Ca^2+-ATPase significantly increased while MDA content reduced markedly in myocardium compared with the model control group. CONCLUSION DK can protect myocardium against ischemia reperfusion injury. The action is perhaps relate to the inhibition of the free radical and subsequent lipid peroxidation.
出处
《中国现代应用药学》
CAS
CSCD
北大核心
2005年第5期364-366,共3页
Chinese Journal of Modern Applied Pharmacy
关键词
地奥心血康
心肌缺血
再灌注损伤
Di'ao Xinxuekang
myocardial ischemia
reperfusion injury