Nrf2基因转染对缺血再灌注心肌炎症反应和氧化应激的影响

[目的]探讨心肌细胞过表达核因子相关因子2（Nrf2）基因后对缺血再灌注损伤导致的炎症反应和氧化应激的影响.[方法]30只SD大鼠随机分成3组（n=10）,A组为对照组,B组为缺血再灌注组,C组为Nrf2组.A组和B组经冠脉转染携带绿色荧光蛋白的腺病毒载体（Ad-EGFP）,C组转染携带Nrf2基因的腺病毒载体（Ad-Nrf2）至心肌组织.稳定3 d后,各组行心肌缺血再灌注损伤（或假实验）.光学显微镜下观察心肌的炎症改变,测定心肌组织超氧化物歧化酶（SOD）活性及丙二醛（MDA）的含量.[结果]缺血再灌注后,光镜下B组亚细胞结构损伤明显,C组结构损伤较B组明显减轻; B、C两组SOD的活性与A组比较明显降低（P〈0.05）,而B组明显低于C组（P〈0.05）;B、C两组MDA含量与A组比较明显升高（P〈0.05）,B组明显高于C组（P〈0.05）.[结论]过表达Nrf2基因能通过抗炎和抗氧化应激保护缺血再灌注心肌.

Effect of Nrf2 Gene Transfection on Inflammatory Response and Oxidative Stress Induced by Myocardial Ischemia Reperfusion Injury

[Objective]To explore the effect of nuclear factor E2 related factor2 （Nrf2） gene transfection on inflammatory response and oxidative stress induced by myocardial ischemia reperfusion injury. [Methods]Thirty SD rats were randomly divided into group A（controlled group）, group B（ischemia-reperfusion group） and group C（Nrf2 group） with 10 rats in each group. Myocardial tissues were transfeeted with recombinant adenovirus vector mediated enhanced green fluorescent protein（Ad-EGFP） via coronary artery in group A and group B. Myocardial tissues were transfected with recombinant adenovirus vector mediated human Nrf2 gene（Ad- Nrf2） in group C. Ischemia reperfusion injury（or sham operation） was induced three days later. The changes of cardiac inflammation response were observed under light microscope. The superoxide dismutase（SOD） activity and malondialdehyde（MDA） content were measured. [Results]After isehemia reperfusion, light microscope showed that subcellular structure was injured obviously. The injury of structure in group C was less than that in group B. Compared with group A, the activity of SOD in group B and group C obviously decreased（ P 〈0.05）, while that in group B was obviously lower than that in group C（ P 〈0.05）. Compared with group A, MDA content in group B and group C obviously increased（ P〈0.05）, while that in group B was obviously higher than that in group C（ P 〈0.05）. [Conclusion]Overexpression of Nrf2 can protect the myocardial tissues from isehemia reperfusion by inhibiting oxidative stress and inflammation response.