碘化N-正丁基氟哌啶醇减轻大鼠心肌缺血再灌注损伤作用的机制研究  

The Protective Effect of N-n-butyl Haloperidol Iodide on Myocardial Ischemia-Reperfusion Injury in Rats

作　　者：贾强用[1] 石刚刚[1] 吕艳秋[1] 陈一村[1] 张艳美[1] 高分飞[1] 

机构地区：[1]汕头大学医学院药理学教研室,广东汕头515041

出　　处：《汕头大学医学院学报》2006年第4期197-200,共4页Journal of Shantou University Medical College

基　　金：国家自然科学基金(30672465)

摘　　要：目的:探讨碘化N-正丁基氟哌啶醇(F2)减轻大鼠心肌缺血再灌注损伤的分子生物学机制。方法:用大鼠在体心肌缺血再灌注模型,通过测定血清中肌酸激酶、乳酸脱氢酶的活性观察心脏损伤的情况;通过测定心肌组织中髓过氧化物酶、超氧化物歧化酶、丙二醛的变化,观察中性粒细胞浸润、氧自由基及脂质过氧化的情况。Western blot法测定心肌缺血组织中早期生长反应基因-1(Egr-1)蛋白水平的变化。结果:与对照组比,反义核苷酸组及反义核苷酸+F2组Egr-1蛋白表达明显减少(P<0.05),炎症反应及心肌损伤程度明显减弱(P<0.05);反义核苷酸+F2组与反义核苷酸组比,Egr-1蛋白表达无统计学意义(P>0.05),心肌损伤及炎症反应程度明显减轻(P<0.05)。结论:F2可通过抑制Egr-1蛋白表达,起到减轻心肌缺血再灌注损伤的作用,除抑制Egr-1蛋白的高表达外,F2还可通过其他机制起到抗心肌缺血再灌注的作用。Objective： To study the mechanism of N-n-butyl halopefidol iodide（ F2 ）attenuating myocardial ischemiareperfusion injury in rats. Methods： The rat experimental models in vivo were established. The system of BL-420 was used to monitor haemodynamics. The levels of creatinkinase, lactic acid dehydrogenase, myeloperoxidase, superoxide dismutase, malondialdehyde were also determined. The expression level of Egr-1 protein in myocardial tissue was exa- mined by Western blot. Results： Compared with the control group, the antisense nucleotide group, antisense nucleotide and F2 group could inhibit the expression levels of Egr-1 protein（ P 〈 0.05）, but there was no difference between the antisense nucleotide group and the antisertse nucleotide and F2 group（ P 〉 0.05）, they beth could protect myocardial tissue from ischemia-reperfusion injury. Conclusion： F2 can protect myocardium from ischemia-reperfusion by inhibiting Egr-1 overexpression, but that is not the whole pharmacological mechanisms of F2.

关 键 词：碘化N-正丁基氟哌啶醇 缺血再灌注损伤 反义核苷酸 早期生长反应基因-1 

分 类 号：R966[医药卫生—药理学]