缺血预处理和吡那地尔预处理对NF-κB的影响及其心肌保护作用  

The influence of preconditioning on the activity of NF-κB and its myocardial protective effects

作　　者：黄燕[1] 刘兴奎[1] 喻田[1] 余志豪[1] 王海英[1] 

机构地区：[1]遵义医学院麻醉教研室,贵州遵义563003

出　　处：《重庆医科大学学报》2006年第3期326-329,共4页Journal of Chongqing Medical University

基　　金：贵州省优秀青年科技人才培养基金(2002-0217)

摘　　要：目的:观察缺血预处理和吡那地尔预处理对心肌核转录因子(NF-κB)活性的影响,进一步探讨预处理心肌保护机制。方法:健康日本大耳白兔80只随机分为5组,分别为空白对照组(C组)、去极化组(K组)、缺血预处理组(I组)、吡那地尔预处理组(P组)和格列本脲阻断组(G组)。建立离体心脏Langendorff模型,待心率平衡10min后全心缺血40min,复灌60min或120min。分别于平衡10min和复灌15min、30min、60min和120min时检测心功能指标;平衡10min和复灌30min时冠脉流量(CF);平衡10min、复灌60min和120min心肌NF-κBP65的表达情况。结果:(1)复灌后I组和P组各项心肌功能和CF恢复率均优于C组和K组(P<0.05或P<0.01)。(2)复灌后60min和120min时,I组和P组心肌细胞胞核NF-κBP65平均灰度值高于C组和K组(P<0.05或P<0.01);G组心肌细胞胞核NF-κBP65平均灰度值较P组降低(P<0.05)。结论:缺血预处理和吡那地尔预处理均能对心肌起到良好地保护作用,其保护机制可能是通过开放ATP敏感性钾通道直接或间接抑制NF-κB激活,进而减轻心肌缺血再灌注损伤。Objective： To investigate the influence of ischemic and pinacidil preconditioning on the activity of NF-κ B and its myocarchalprotective effects. Methods： Eighty isolated rabbit hearts were randomized into five groups （Group C ,K,I,P,G）. Hearts were removed andmounted in a Langendorff apparatus perfused with 37℃ oxygenated Krebs-Henselet buffer. All groups were subjected to gobal myocardialischemia for 40 rain and reperfusion for 60 min or 120 min. Cardiac functions were monitored at 10 rain equilibration , 15 min ,30 min ,60min and 120 min reperfusion; Coronary flow （CF） was measured at 10 rain equilibration and 30 min reperfusion; Expression of NF- κ BP65 was determined at 10 rain equilibration ,60 rain and 120min reperfusion. Results： （1）After ischemic reperfusion, the recovery of cardiac function and CF in Group I and Group P was significantly superior to that in Group C and Group K （P〈 0.01 or P〈 0.05）; （2） The expression of NF- κ B P65 in Group I and Group P was greater than that in Group C and Group P; The expression of NF-κ B P65 in GroupG were higher than that in Group P （ P 〈 0.05）. Conclusion： Both ischemic and pinacidil preconditioning can protect myocardium frommyocardial inflammation during ischemic reperfusion, the mechanisms of which may be that the opening sensitive potassium channel mighthave inhibited the activation of NF- κ B directly or indirectly.

关 键 词：缺血再灌注损伤 预处理 ATP敏感性钾通道 核转录因子κappaB 

分 类 号：R654.2[医药卫生—外科学]