目的 探讨肢体远端缺血预处理对老龄大鼠肝脏热缺血再灌注损伤及核因子E2相关因子(Nrf2)信号通路的影响.方法 将12只雄性Sprague-Dawley大鼠随机分为预处理组和对照组.建立老龄大鼠(15 ~16月龄)70%肝脏热缺血再灌注模型(缺血1h,再灌注2h),分别于术后检验血清ALT水平变化并采集肝脏组织测定丙二醛(MDA)含量以及抗氧化酶-超氧化物歧化酶(SOD)活性,观察肝组织病理学改变,应用Western blot检测肝组织核转录因子E2相关因子(Nrf2)蛋白的变化.结果 预处理组大鼠血清ALT、肝组织MDA水平明显低于对照组(P<0.05).预处理组大鼠的肝脏病理损伤较对照组轻.与对照组相比,预处理组大鼠肝组织Nrf2蛋白表达水平、SOD活性升高(P<0.05).结论 远端缺血预处理能够减轻老龄大鼠70%肝脏热缺血再灌注损伤后,其作用机制可能与其激活Nrf2信号通路有关.
Objective To investigate the effect of remote ischemic preconditioning on nuclear factor erythroid-2 related factor 2 (Nrf2) signaling in the liver of aged rats after warm ischemia reperfusion injury.Methods A 70% hepatic warm ischemia-reperfusion model was established in aged rats (15-16 months old) (1 hour after ischemia and 2 hours after reperfusion).12 male Sprague-Dawley rats were divided into two groups:pretreatment group and control group.The level of serum alanine aminotransferase (ALT) was detected after operation and the liver tissues were harvested for the determination of malondialdehyde (MDA) content and the activity of antioxidant enzyme-superoxide dismutase (SOD).The pathological changes of liver were observed.The change of Nrf2 protein expression in liver tissue was examined by Western blot.Results Serum ALT and MDA in the pretreatment group were significantly lower than those in the control group.The liver pathological damage of pretreatment group rats were lighter than the control group (P < 0.05).Compared with the control group,the Nrf2 protein expression and the activity of SOD increased in the liver of pretreatment group (P < 0.05).Conclusions Remote ischemic preconditioning can reduce 70% hepatic ischemia-reperfusion injury in aged rats,and its mechanism may be related to its activation of Nrf2 signaling pathway.