【摘要】 目的:观察青蒿素(AS)对离体大鼠心肌缺血/再灌注损伤的保护作用并初步探讨其可能机制。方法:Wistar大鼠50只,随机分成正常对照组、缺血/再灌注损伤组(I/R)和AS组(10,100,1000μmol.L-1)(n=10)。利用Langendorff离体灌流装置,复制大鼠心肌缺血/再灌注损伤模型。观察指标:心电图、心功能参数、冠脉流量、心肌组织匀浆中乳酸脱氢酶(LDH)、肌酸激酶(CPK)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量及心肌超微结构等。结果:AS(10,100μmol.L-1)可明显改善缺血/再灌注后的心肌功能(±dp/dtmax,LVSP)指标,增加冠脉流量,减少LDH和CPK的漏出,同时,可使SOD活性升高和MDA含量降低及心肌超微结构损伤减轻。当AS浓度达到1000μmol.L-1时,未见保护作用。结论:中、低剂量AS(10,100μmol.L-1)能减轻大鼠心肌缺血/再灌注损伤,其机制可能与AS具有抗氧化和清除自由基的作用有关。更多还原

【Abstract】 Objective: To observe the effect of artemisinin on the ischemia/ reperfusion injury of the iisolated rat myocardium and to preliminarily study the possible mechanism.Method: Fifty Wistar rats were randomly divided into 5 groups: a control group,an ischemia/reperfusion(I/R) group,and 3 artemisinin(AS) groups(10,100,1 000 μmol·L-1),10 rats in each group.Ischemia/reperfusion injury of the isolated rat myocardium was induced by a Langendorff system.The electrocardiogram,the cardiac functional parameters,coronary flow,and the activities of LDH(lactate dehydrogenase),CPK(creatine phosphokinase),SOD(superoxide dismutase) and the level of malondiadehyde(MDA) in myocardial tissue,and the myocardial ultrastructures were investigated.Result: AS(10,100 μmol·L-1) could significantly improve the index of the myocardial function(±dp/dtmax,LVSP)after the ischemia/reperfusion,increase the coronary flow, decrease the leakage of LDH and CPK,and increase the SOD activity and decrease the MDA level in cardiac tissues,and alleviate the myocardial ultrastructure injury.But,AS(1 000 μmo·L-1) did not have the above effects.Conclusion: AS(10,100 μmol·L-1) alleviate the myocardial ischemia/reperfusion injury in rats.The mechanism may be related to its functions of antioxidation and scavenging free radicals.更多还原