摘要
目的观察参附注射液对大鼠心肌缺血再灌注后组织损伤的影响,并从核转录因子E2相关因子2(Nrf2)/血红素加氧酶(HO)-1信号通路研究其作用机制。方法 SD大鼠随机分为正常对照组、假手术组、模型对照组、参附注射液组。术前1d、术前1h和术后1h尾静脉给药,共3次,结扎大鼠左冠状动脉前降支30min,制造心肌缺血模型,再灌注60min后,行NBT染色测心肌梗死面积,检测心肌组织中氧自由基丙二醛(MDA)及超氧化物歧化酶(SOD)的水平,以及心肌组织中HO-1蛋白及HO-1 m RNA的表达水平。结果缺血再灌注60min后,参附注射液组较模型组心肌组织梗死程度减轻,HO-1表达增强,且心肌组织SOD含量高于模型组,MDA则低于模型组。结论参附注射液具有抗心肌缺血再灌注损伤的作用,其机制可能与激活Nrf2/HO-1信号途径,促进下游抗氧化蛋白HO-1的表达,从而激活和保护内源性氧自由基清除剂SOD活性,灭活氧自由基MDA有关。
Objective To investigate the effects of the Shenfu injection on oxidative stress and nuclear factor-erythroid2 related factor 2（Nrf2）/heme oxygenase（HO）-1 pathway after acute myocardial ischemia-reperfusion injury in rats. Methods Adult male SD rat were randomly divided into 4 groups of normal,sham,model control,Shenfu injection. Treated for 1 d before surgery,1 h before surgery and 1 h after surgery,myocardial ischemia-reperfusion injury was established by left coronary artery ligation for 30 min followed by reperfusion for 60 min, malondialdehyde（MDA）, superoxide dismutase（SOD）,HO-1 m RNA and HO-1 protein expression in tissues were determined.Results After myocardial ischemia-reperfusion for60 min,the degree of infarction of myocardial infarction in Shenfu injection group was reduced. The contents of MDA was increased,SOD activity was decreased,at the same time,HO-1 m RNA and HO-1 protein expression in myocardial tissues was significantly up-regulated. Conclusion Shenfu injection can strengthen the antagonism effects on oxidative stress injury after myocardial ischemic-reperfusion. The underlying mechanism may be associated with activating Nrf2/HO-1 signal transduction pathway,then advancing the expression of antioxidantgene in the downstream such as HO-1.
作者
李倩
王智超
LI Qian;WANG Zhichao(Department of Emergency, Wuhan No. 1 Hospital, Wuhan 430022)
出处
《湖北中医药大学学报》
2018年第3期17-20,共4页
Journal of Hubei University of Chinese Medicine
基金
湖北省武汉市卫生计生委科研基金(项目编号:WZ16C12)
