NF-кB参与七氟烷预处理所致延迟性抗大鼠心肌缺血再灌注损伤

NF-кB participates in sevoflurane preconditioning induced delayed type protection against ischemia-reperfusion injury in myocardium of rats

目的观察七氟烷预处理对大鼠心肌缺血再灌注损伤的延迟性保护作用,探讨NF-κB参与保护作用的机制。方法雄性SD大鼠随机分为:对照组(CON组);缺血再灌注组(I/R组);七氟烷延迟性组(SWOP组);七氟烷对照组(SEVO组);PTN(NF-кB特异性阻断剂)组;DMSO组以及PTN+SWOP组。用TTC染色法测定心肌梗死范围;Western blot法检测NF-кB(P65,P50)蛋白表达。结果与I/R组相比SWOP组梗死范围减小,且该作用可被PTN所阻断;SWOP组缺血前NF-кB(P65,P50)蛋白表达(56±4,58±3)高于CON组(34±4,40±1);I/R和SWOP组再灌注后NF-кB(P65,P50)蛋白表达均上调,SWOP组蛋白上调幅度低于I/R组。结论七氟烷预处理对大鼠心肌缺血再灌注损伤具有延迟性保护作用;NF-кB可能参与了其延迟性保护机制。

Objective To investigate the delayed protection of sevoflurane preconditioning（SWOP） against myocardium ischemia/reperfusion（I/R） injury and the mechanism of NF-кB during SWOP.Methods Adult male Sprague-Dawley rats were randomly assigned to receive 33% oxygen（I/R group） with or without 2.5% sevoflurane for 2 h（SWOP group）.The NF-κB inhibitor parthenolide（500 μg/kg） was intraperitoneally administered before sevoflurane exposure（PTN＋SWOP group）.Infarct size was measured by TTC staining.The related proteins of NF-κB were determined with Western blot.Results Sevoflurane significantly reduced infarct size,and this effect was blocked by PTN.Sevoflurane up-regulated the expression of NF-кB（P65,P50） proteins compared with CON group before ischemia.The expression of NF-кB（P65,P50） proteins were up-regulated in I/R and SWOP group compared with CON group after reperfusion,but they were lower in SWOP group.Conclusions Preconditioning with sevoflurane reduces myocardial infarct size,produces SWOP.NF-κB may play an important role in the mechanism of SWOP against myocardium I/R injury.