HO-1在缺血后处理抗肺缺血再灌注损伤中的作用及其对STAT-3表达的影响

目的 研究血红素加氧酶-1（hemeoxygenase-1，HO-1）在缺血后处理（ischemic postconditioning，IPO）抗肺缺血再灌注损伤中的作用机制及其对STAT-3蛋白表达的影响。方法 40只SD雄性大鼠（250-280 g）随机分为假手术组（S）、缺血再灌注组（IR）、缺血后处理组（IPO）及缺血后处理 HO-1抑制剂组（IPO ZnPP）。称重法计算缺血肺组织干/湿比（W/D），试剂盒检测缺血肺组织MDA水平及MPO与HO-1活性，Western Blot检测HO-1，p-STAT-3蛋白表达水平。结果 与S组比较，IR组大鼠W/D、MDA、MPO、HO-1活性及蛋白表达水平均显著增加，而p-STAT-3蛋白表达水平显著降低，IPO可以逆转上述变化，而HO-1特异性抑制剂可以取消IPO对上述指标的影响。结论 IPO可以通 过促进HO-1活性及蛋白表达的增加从而激活STAT-3信号通路而发挥抗肺缺血再灌注损伤作用。

Ischemic postconditioning attenuates lung ischemia-reperfusion injury by hemeoxygenase-1 induced STAT-3 activation in rats

To study the mechanisms of hemeoxygenase-1 (HO-1) in ischemic postconditioning attenuating lung ischemia reperfusion injury and its effects on STAT-3 in postischemic lung of rats. Methods: Forty male SD rats were randomly assigned to shame group (S), ischemia-reperfusion injury group (IR), ischemic postconditioning group (IPO) and IPO with HO-1 inhibitor ZnPP treatment group (IPO ZnPP). The ratio of dry / wet weight (W/D), the level of MDA, and the activity of MPO and HO-1 were measured in postischemic lung tissures. The protein expression of HO-1 and p-STAT-3 were detected by Western blot. Results: The levels of W/D, MDA, MPO, HO-1 activity and its protein expression were all significantly increased as compared with the S group, while the expression level of p-STAT-3 protein was significantly decreased, IPO can reverse these changes, and the specific inhibitor of HO-1 Znpp canceled the effects of IPO on the above indexes. Conclusion: IPO attenuates lung ischemia-reperfusion injury by promoting HO-1 induced activation of STAT-3 signaling pathway.