北五味子乙素对大鼠心肌缺血再灌注损伤的保护作用

Protective Effect of Schisandrin B on Myocardial Ischemia/Reperfusion Injury in Rats

目的:观察北五味子乙素(schisandrin B,Sch B)对大鼠心肌缺血再灌注损伤(myocardial ischemia/reperfusion injury,MI/RI)的保护作用及其作用机制,为研发疗效确切、抗心肌缺血作用的保健成分提供理论依据。方法:60只雄性Wistar大鼠随机分为6组:假手术组,MI/RI组,Sch B 20、40、80 mg/(kg·d)剂量组,阳性对照(美托洛尔(metoprol,MET),2.5 mg/(kg·d))组。各组灌胃给药3周后建立大鼠缺血再灌注损伤模型,肉眼观察大鼠心脏组织变化,采用四氮唑硝基蓝(nitro blue tetrazolium,NBT)染色法测定大鼠心肌梗死面积,利用全自动生化分析仪测定大鼠血清中杂化型肌酸激酶同工酶(creatine kinase-MB,CK-MB)、乳酸脱氢酶(lactic dehydrogenase,LDH)、超氧化物歧化酶(superoxide dismutase,SOD)活力以及丙二醛(malonaldehyde,MDA)、一氧化氮(nitric oxide,NO)水平,使用生物信号采集处理系统测定大鼠心脏功能指标变化,显微镜下观察大鼠心肌病理学改变状况。结果:Sch B能够明显减轻MI/RI造成的大鼠心脏损伤,减小心肌梗死面积,提高大鼠血清中SOD活力和NO水平,降低MDA含量和CK-MB、LDH活力,改善大鼠心肌功能。结论:Sch B对大鼠MI/RI有一定的保护作用,其机制可能与减少氧自由基释放、保护缺血心肌免受MI/RI有关。

Objective： To investigate the protective effect of schisandrin B（Sch B） on myocardial ischemia/reperfusion injury（MI/RI） and its underlying mechanism so as to provide theoretical basis for new drug development of traditional Chinese medicine（TCM） with defined activity and high efficiency against myocardial ischemia. Methods： Totally 60 male Wistar rats were randomly divided into six groups： control group, reperfusion injury（MI/RI） group, Sch B 20, 40 and 80 mg/（kg·d） dose groups and positive control drug metoprolol group（MET, 2.5 mg/（kg·d））. Drug intragastric（ig） administration was continued for three weeks before ischemia-reperfusion injury. General heart change and myocardial pathological change were observed, Evans blue and NBT staining was conducted to determine infarction area, and changes in serum enzymes and cytokines and cardiac function were measured at the end of the experiment. Results： Sch B could significantly alleviate heart damage induced by MI/RI, reduce the infarction area, elevate SOD and NO levels in serum, reduce MDA, CK-MB and LDH contents, improve myocardial function. Conclusion： Sch B has certain protective effects against myocardial ischemia-reperfusion injury in rats, and its mechanism may be related to reducing oxygen free radical release and protecting ischemic myocardium from MI/RI.