在体大鼠心肌缺血再灌注损伤中NF-κBp65与AngⅡ的关系

Studies on interaction between NF-κBp65 and AngⅡ during myocardial ischemia-reperfusion injury in rats

目的初步探讨心肌缺血再灌注损伤(IRI)过程中NF-κBp65与血管紧张素Ⅱ(AngⅡ)的关系。方法建立在体大鼠心肌IRI模型。以缺血30min再灌注60min(I30minR60min)为观察点,采用随机数字表法分为IR组(即I30minR60min后不再经任何处理)、PDTC预处理组、咪达普利预处理组、PDTC与咪达普利联合预处理组。分别通过酶联免疫吸附试验(ELISA)及放射免疫分析法检测NF-κBp65活性及血浆和心肌组织中的AngⅡ含量。通过析因分析观察NF-κBp65与AngⅡ的相关性。结果各药物预处理组与IR组比均可抑制NF-κBp65活性及血浆和心肌组织中的AngⅡ含量,差异有统计学意义(P<0.05)。结论心肌缺血再灌注损伤过程中NF-κBp65与AngⅡ相互激活,形成正反馈,共同加重此损伤病理过程。

Objective Utilizing the characters of pyrrolidine dithiocarbamate known as a specific inhibitor of NF‐κB and imidapril known as a specific inhibitor of angiotensin converting enzyme ,this study was to initially investigate the relationship between NF‐κBp65 and AngⅡ during the process of myocardial ischemia reperfusion injury .Methods Rat models of myocardial ischemia reper‐fusion injury were successfully established .The observation point is 60 min of reperfusion after 30 min（I30 min R60 min ） ischemia ,the DNA activate of NF‐κBp65 was detected by ELISA ;the content of AngⅡ in blood plasma and cardiac were determined by radioim‐munoassay .We pretreated with pyrrolidine dithiocarbamate ,imidapril ,and both of them to observe changes of the same indexs .Re‐sults Compared with I30 min R60 min ,Pyrrolidine dithiocarbamate ,Imidapril and pyrrolidine dithiocarbamate add imidapril could all ob‐viously inhibit NF‐κBp65 activation and depress the content of Ang Ⅱ in blood plasm and cardiac ,the pyrrolidine dithiocarbamate add imidapril was most obviously .Conclusion During the process of myocardial ischemia‐reperfusion injury ,NF‐κBp65 had been activated ,and the content of Ang Ⅱ in blood plasm and cardiac had increased .NF‐κBp65 and AngⅡ could influence and promote each other during myocardial ischemia reperfusion injury .