远隔缺血后处理对大鼠深低温肺缺血再灌注损伤的保护机制研究

目的 初步探讨远隔缺血后处理对在体大鼠肺深低温缺血再灌注损伤的保护作用及Nrf2在其中的作用机制。方法 建立大鼠深低温肺缺血再灌注模型，在此模型基础上进行远隔缺血后处理干预及阻断Nrf2信号通路，检测不同处理条件下肺组织中丙二醛（malondialdehyde，MDA）含量、超氧化物歧化酶（superoxide，SOD）活性、肺湿/干重比值（W/D）、Western blot法测定Nrf2的表达情况和肺组织HE染色光镜观察。结果 远隔缺血后处理组较缺血再灌注组肺组织Nrf2表达增加（P<0.05）肺损伤程度明显减轻，MDA含量减少（P<0.05），SOD活性增高（P<0.05），W/D比值减低；而阻断Nrf2信号通路后这一变化明显减弱。结论 远隔缺血后处理能减轻大鼠深低温肺缺血再灌注损伤程度，Nrf2信号通路可能参与深低温肺缺血远隔缺血后处理的保护机制。

Protection Mechanism Research of Remote Ischemic Postconditioning in Rats with Deep Hypothermic Lung Ischemia-reperfusion Injury

Objective To explore the protective effect of remote ischemic postconditioning in the deep hypothermia ischemic-reperfusion injury of rat lung,and study the role of Nrf2 signaling pathway in remote ischemic postconditioning. Methods Deep hypothermic lung ischemia-reperfusion model was set up. Intervention by the model was made by remote ischemic postconditioning and blocking Nrf2 signaling pathway.The Nrf2 protein expression,MDA content,SOD activity and Wet and dry ratio of lung was detected. Results Compared with the I/R group, Nrf2 expression and SOD activity were increased in RIPO group,while the MDA content and W/D ratio were decreased.And this change in blocking Nrf2 signaling pathway significantly reduced. Conclusion The RIPO can reduce lung ischemic-reperfusion injury of rat which in deep hypothermia,the Nrf2 signaling pathway may be involved in the protective effects induced by RIPO.