黄芪多糖对心肌缺血再灌注损伤心肌P38信号通路的影响  

Effects of Astragalus Polysaccharides on Myocardial P38 Signal Pathway During Myocardial Ischemia Reperfusion Injury

作　　者：王加良[1] 丁禄荣[1] 丛军兹[1] 尹昌浩[1] 

机构地区：[1]牡丹江医学院附属红旗医院,黑龙江牡丹江157011

出　　处：《牡丹江医学院学报》2017年第3期14-16,共3页Journal of Mudanjiang Medical University

基　　金：牡丹江医学院科学技术研究项目(2011-19)

摘　　要：目的实验研究黄芪多糖(APS)对心肌缺血再灌注损伤心肌P38信号通路所具有的影响。方法选取Wistar大鼠70只,随机划分为假手术组、缺血再灌注模型组、APS高剂量+SB203580组、APS低剂量+SB203580组、p38MAPK阻断剂(SB203580)组、APS高剂量组及APS低剂量组,各组10只。运用结扎左冠状动脉前降支对缺血再灌注损伤模型进行复制。将相应药物注射于各组大鼠尾声静脉,1次/d。持续30d。采用四氮唑蓝染色氯化硝基后,对梗死重量及心肌梗死面积进行测量。结果相比于模型组,除APS低剂量组外,其余各组均可实现缺血再灌注心肌重量及梗死面积的明显减少(P<0.05),且APS高剂量与SB203580组联合治疗,效果相比于各单药治疗组,优于后者且差异显著(P<0.05)。结论 APS可对大鼠心肌缺血再灌注损伤情况给予显著改善,p38MAPK阻断剂与APS高剂量联合运用,能够对再灌注损伤的抑制具有良好的协同作用,其作用机制可能是对p38MAPK信号通路予以部分抑制,对其介导的炎症反应进行阻断进而损伤心肌相关。Objective The effects of APS on myocardial P38 signal pathway after myocardial ischemia / reperfusion injury were studied. Methods Selected 70 Wistar rats were randomly divided into sham operation group, ischemia reperfusion model group and APS high dose group,low dose ＋ SB203580 APS ＋ SB203580 group,p38MAPK inhibitor （SB203580） group and APS high dose group and APS low dose group, 10 rats in each group. The left anterior descending coronary artery was ligated to make the model of ischemia - reperfusion injury. The corresponding drugs were injected into tail vein of each group, 1 time / d. Sustained 30d. The infarct size and myocardial infarct size were measured after nitroglycerin staining with tetrazolium. Results Compared with the model group, the weight and infarct size of isehemic reperfused myoeardium decreased significantly （ P 〈 0.05 ） in the other groups except APS low dose group, and the combination of APS and SB203580 （ P 〈 0.05 ） , compared with the single drug treatment group, the difference was significant （ P 〈 0.05 ）. Conclusion APS can significantly improve myocardial ischemia - reperfusion injury in rats, p38MAPK blocker and APS high -dose combination, can inhibit the inhibition of reperfusion injury has a good synergies ,and its mechanism may be p38MAPK signaling pathway to be Partial inhibition of its mediated inflammatory response to block and thus myocardial damage.

关 键 词：黄芪多糖 心肌缺血再灌注 心肌P38信号通路 影响 

分 类 号：R73[医药卫生—肿瘤]