摘要
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特异性抑制剂可以消除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。
Objective To study the mechanisms of hemeoxygenase-1 （ HO-1 ） in ischemic postconditioning attenu- ating pulmonary ischemia reperfusion injury and its effects on STAT-3 in isehemia reperfusion injury in the rat lungs. Methods Forty male SD rats were randomly assigned to shame group （S）, ischemia-reperfusion injury group （IR）, is- chemic postconditioning group （IPO） and IPO with HO-1 inhibitor ZnPP treatment group （IPO ＋ ZnPP）. The ratio of dry/ wet weight （W/D） , level of MDA, and activity of MPO and HO-1 were measured in the postischemic lung tissues. The ex- pression of HO-1 and p-STAT-3 proteins were detected by Western blot. Results The W/D, MDA, MPO, HO-1 activity and expression of HO-1 protein in the IR group were all significantly increased as compared with those in the group S, while the expression level of p-STAT-3 protein was significantly decreased. IPO could reverse these changes, and Znpp, the spe- cific inhibitor of HO-1, could abolish the effects of IPO on the above indexes. Conclusions IPO attenuates the pulmonary isehemia-reperfusion injury by promoting HO-1 induced activation of STAT-3 signaling pathway.
出处
《中国实验动物学报》
CAS
CSCD
2013年第4期81-85,共5页
Acta Laboratorium Animalis Scientia Sinica
