【摘要】 目的:探讨碘化N-正丁基氟哌啶醇(F2)对缺氧复氧心肌细胞损伤及早期生长反应基因-1(Egr-1)蛋白表达的影响。方法:用1~3 d的SD大鼠进行心肌细胞原代培养,取生长5~6 d的心肌细胞分为对照组、缺氧复氧组、聚乙二醇+脂质体组、反义寡核苷酸组、反义寡核苷酸+F2组,除对照组外其他组均做缺氧复氧模型。通过测定肌酸激酶、乳酸脱氢酶、肌钙蛋白、超氧化物歧化酶、丙二醛及肿瘤坏死因子-α的变化,观察心肌细胞损伤及炎症反应情况;Western blot法检测培养心肌细胞中Egr-1蛋白的表达水平。结果:与对照组比,反义寡核苷酸组及反义寡核苷酸+F2组Egr-1蛋白表达明显减少(P<0.05),细胞损伤及炎症反应程度明显减弱(P<0.01);反义寡核苷酸组与反义寡核苷酸+F2组比,Egr-1蛋白表达虽无统计学意义(P>0.05),但细胞损伤及炎症反应改善情况却有统计学意义(P<0.05)。结论:F2可通过抑制Egr-1蛋白表达来减轻缺氧复氧心肌细胞的损伤,它还可通过其他机制起到保护缺氧复氧心肌细胞损伤的作用。更多还原

【Abstract】 Objective:To study the effects of N-n-butyl haloperidol iodide（F₂）on early growth response gene-1（Egr-1）protein expression in cultured cardiocytes after hypoxia/reoxygenation.Methods:The cardiocytes from neonatal SD rats were isolated and cultured.The hypoxia/reoxygenation models of neonatal rat cardiocytes were established.The cardiocytes were randomly divided into control group,hypoxia/reoxygenation group,Macrogol and Lipfectemine group,antisense nucleotide group,antisense nucleotide and F₂ group.Levels of creatinkinase,lactic acid dehydrogenase,troponin,superoxide dismutase,malondialdehyde,tumour necrosis factor-α were determined.The expression levels of Egr-1 protein in cardiocytes were examined by Western blot.Results: Compared with the control group,antisense nucleotide group and antisense nucleotide and F₂ group could inhibit the expression levels of Egr-1 protein（P<0.05）,but there was no difference between antisense nucleotide group and antisense nucleotide and F₂ group（P>0.05）.Conclusion: F₂ can protect cardiocytes from hypoxia/reoxygenation injury by inhibiting Egr-1 overexpression,but that is not the whole molecular mechanisms of F₂.更多还原