黄芪多糖对大鼠心肌缺血再灌注损伤心肌p38信号通路的影响

目的 研究黄芪多糖(APS)对大鼠缺血再灌注损伤心肌的作用.方法 将70只Wistar大鼠随机分为假手术组、缺血再灌注模型组、APS低剂量组、APS高剂量组、p38MAPK阻断剂(SB203580)组、APS低剂量+SB203580组、APS高剂量+SB203580组,每组10只.采用结扎左冠状动脉前降支复制缺血再灌注损伤模型.各组大鼠尾声静脉注射相应药物,每日1次,连续给药30天.氯化硝基四氮唑蓝染色后,测量心肌梗死面积及梗死重量.结果 与模型组比较,除APS低剂量组外,其他各给药组均可显著减少缺血再灌注心肌的梗死面积和重量(P＜0.05或P＜0.01),并且APS高剂量联合SB203580组治疗效果明显优于各单药治疗组(P＜0.05).结论 APS能够明显改善大鼠心肌缺血再灌注损伤,APS高剂量与p38MAPK阻断剂联合应用对抑制再灌注损伤具有协同作用,其机制可能与其部分抑制p38MAPK信号通路,阻断其介导的炎症反应对心肌的损伤有关.

Effect of Astragalus Polysaccharide on p38 MAPK Signal Pathway of Rats with Myocardial Ischemic Reperfusion Injury

Objective To study the effect of astragalus polysaccharide (APS) on myocardial ischemic reperfusion injury in rats.Methods Seventy Wistar rats were randomized into sham operation group,model group,APS low dose group,APS high dose group,p38MAPK SB203580 group,APS low dose & SB203580 group,and APS high dose & SB203580 group,with 10in each.The left anterior descending coronary artery was ligated to make models of ischemic reperfusion injury.The corresponding medicine was injected via tail vein of each group of rats,once a day,30 days in total.The size and weight of the infarcted myocardium were measured after nitro blue tetrazolium chloride dyeing.Results Infarcted size and weight of the ischemic reperfusion myocardium were lower in all groups except the APS low dose group than in the model group (P<0.05 or P<0.01).Furthermore,the APS high dose &SB203580 group had better effect than other groups (P<0.05).Conclusion APS is effective in improving the pathological condition of myocardial ischemic reperfusion injury in rats,and the combination of APS high dose with SB203580 has a synergic function in inhibiting the reperfusion injury.The mechanism may be related to its effect in inhibiting the p38MAPK signal pathway and blocking the induced inflammatory reaction on myocardium.