远隔缺血后适应对大鼠脑缺血再灌注损伤的作用及相关机制研究

目的探讨远隔缺血后适应对大鼠脑缺血再灌注损伤的作用及相关机制。方法将36只雄性SD大鼠随机数字表法分为3组—对照组(缺血再灌注损伤组)、实验1组(缺血预适应+缺血再灌注损伤组)与实验2组(远隔缺血后适应+缺血再灌注损伤组),每组各12只大鼠。在实验后3 d观察大鼠的一般状况,并测定超氧化物歧化酶(SOD)活力、组织凋亡与Caspase-3蛋白表达水平。结果3组大鼠在建模过程中有6只因建模失败而死亡,3组建模后3 d存活大鼠的体温、体重等比较,差异无统计学意义(P>0.05);而实验后3 d,实验1组与实验2组的脑组织凋亡指数、脑梗死面积、脑组织Caspase-3蛋白表达水平和血清SOD活力均显著低于对照组,体重均显著高于对照组(P<0.05),实验1组与实验2组比较差异无统计学意义(P>0.05)。结论远隔缺血后适应后,脑缺血再灌注损伤大鼠脑梗死面积显著减小,其原因可能与远隔缺血后适应可抑制Caspase-3蛋白表达以及脑组织细胞凋亡,并降低SOD活性有关,而缺血预适应与远隔缺血后适应对脑缺血再灌注影响无显著差异。

Study on the effects of remote ischemic adaptation on cerebral ischemia-reperfusion injury in rat and the related mechanism

Objective To explore the effects and mechanism of remote ischemic adaptation on cerebral ischemia-reperfusion injury in rat.Methods According to random number table method,36 male SD rats were divided into three groups-control group(ischemia-reperfusion injury group),experiment 1 group(ischemic preconditioning+ischemia-reperfusion injury group)and experiment 2 group(distance after ischemia and adaptation)+ischemia-reperfusion injury group),12 rats in each groups.The general condition of the rat were observed 3 days after the experiment,the superoxide dismutase(SOD)levels,tissue apoptosis,and Caspase-3 protein expression levels were determined.Results During the modeling process,there were 6 caess of rat in the three groups were died due to the failure of modeling.There were no statistically significant difference in body temperature and weight compared among the 3 groups of rat after 3 days of modeling(P>0.05).And 3 days after the intervention,the cardiac tissue apoptosis index,cerebral infarction area,the expression level of Caspase-3 protein and the activity of serum SOD in brain tissue were significantly lower than those of the control group(P<0.05),and the weight of rats was significantly higher than that of the control group(P<0.05),there were no statistically significant difference compared between the experimental group 1 and experimental group 2(P>0.05).Conclusion After adaptation after remote ischemia,the cerebral infarct area of rats with cerebral ischemia-reperfusion injury was significantly reduced.The reason may be related to that adaptation after remote ischemia can inhibit the expression of Caspase-3 protein and the apoptosis of brain tissue cells,and reduce the activity of SOD.But there was no significant difference in the effects of ischemic preconditioning and remote ischemic postconditioning on cerebral ischemia reperfusion.