尤瑞克林对大鼠局灶性脑缺血再灌注损伤后APE/Ref-1表达的影响

Effect of Urinary kallikrein on the expression of apurinic apyrimidinic endonuclease/redox factor 1(APE/Ref-1) in cerebral tissue of rats subjected to cerebral ischemic-reperfusion injury

目的探讨尤瑞克林对大鼠局造性脑缺血再灌注损伤(I/R)后无嘌呤/无嘧啶核酸内切酶/氧化还原因子1(APE/Ref-1)表达的影响,进一步探讨尤瑞克林脑保护作用的机制。方法健康成年雄性SD大鼠54只,采用随机数字表法分为3组:空白对照组(Con组)(n=18),局造性脑缺血再灌注组(Mod组)(n=18),尤瑞克林干预组(URK组)(n=18),每组随机各取6只分别用TTC染色检测大鼠脑梗死体积;Western blot检测海马组织中APE/Ref-1的表达;免疫组化检测海马组织中CA1区APE/Ref-1阳性细胞数。结果与Con组相比,Mod组大鼠海马组织APE/Ref-1蛋白的表达量明显下降,海马CA1区APE/Ref-1阳性细胞数明显下降(P<0.05);尤瑞克林组能显著提高APE/Ref-1的表达量及提高APE/Ref-1阳性细胞数,但低于Con组(P<0.05),尤瑞克林能减少大鼠的脑梗死体积(P<0.05)。结论尤瑞克林能提高大鼠局造性脑缺血再灌注损伤后APE/Ref-1的表达,这可能是尤瑞克林脑保护作用的又一机制。

ObjectiveTo investigate the effect of Urinary kallikrein on the expression of apurinic apyrimidinic endonuclease/redox factor 1 （APE/Ref-1） in rats which were subjected to reperfusion after middle cerebral artery occlusion （MCAO） for two hours. To explore the protective mechanism of Urinary kallikrein against ischemic/reperfusion brain injury.Methods 54 male Sprague-Dawley rats were randomly divided into three groups with 18 mice each group： control group （Con group）, ischemic/reperfusion group （Model group）, ischemic/reperfusion plus Urinary kallikrein group （URK group）. Six rats from each group randomly selected were respectively subjected to the detection of APE/Ref-1 positive cell count in CA1 region of hippocampus by immunohistochernistry, the detection of cerebral infarct volume by TTC staining and the detection of the expression of protein APE/Ref-1 in hippocampus by Western blot.ResultsCompared with Con group, the levels of protein of expression of APE/Ref-1 in hippocampus significantly decreased （P〈0.05）, with the APE/Ref-1 positive cell count in CA3 region of hippocampus significantly lower （P〈0.05）, Urinary kallikreincan increase the protein of expression of APE/Ref-1 and the APE/Ref-1 positive cell count in CA1 region of hippocampus, but lower than that of Con group, Urinary kallikrein can decrease thecerebral infarct volume induced by the reperfusion after middle cerebral occlusion （MCAO）.ConclusionUrinary kallikreincan increase the protein of expression of APE/Ref-1 after focal cerebral ischemia/reperfusion, that may be the other protective mechanism of Urinary kallikrein against ischemic/reperfusion brain injury.