【摘要】 目的 :应用大鼠心肌缺血再灌注模型观察碘化N 正丁基氟哌啶醇 (N n butylhaloperidoliodide ,F2 )对早期生长反应蛋白 1(earlygrowthresponse 1,Egr 1)转录及表达水平的影响 ,及其对心肌炎症及心功能的改善作用。方法 :结扎大鼠冠状动脉左前降支 ,制成急性心肌缺血再灌注损伤模型 ,缺血前5min ,舌下静脉推注F2 ,监测血流动力学的变化 ,病理组织切片观察缺血心肌组织炎性反应变化。应用RT PCR方法及Western blot方法分别检测缺血组织Egr 1mRNA及蛋白水平变化。结果 :与对照组相比 ,F2 治疗组心肌组织内炎性反应及Egr 1的转录与表达均降低 ,心肌功能也得到明显改善。结论 :F2具有明显抑制缺血再灌注大鼠心肌组织内Egr 1mRNA及蛋白表达、减轻炎性损伤的作用 ,这可能是F2 对心肌缺血再灌注损伤显著保护作用的机制之一。更多还原

【Abstract】 AIM: To investigate the effects of N-n-but yl haloperidol iodide (F 2) on Egr-1 mRNA and protein expression in the model of rats with myocardial ischemia-reperfusion. METHODS: The myocar dial ischemia-reperfusion injury animal model was established by occluding rat ’s left anterior descending branch of coronary artery for 60 min and later open ing the ligation to reperfusion for 180 min in vivo. F 2 were a dministered by intravenous injection before the onset of ischemia for 5 min. The changes of hemodynamics were recorded during the experiment, and then the ische mia tissue was extract. The inflammation was observed by tissue section. The Egr -1 gene transcription and protein expression were detected by RT-PCR and Weste rn-blot, respectively. RESULTS: F 2 reduced the levels of Egr -1 mRNA and protein, relieve inflammation and ameliorate the hemodynamics of is chemia-reperfusion injured myocardium. CONCLUSION: F 2 can rel ieve inflammatory injury and protect myocardial function in rats with myocardial ischemia-reperfusion, and the mechanism may be related to attenuating the tran scription and expression of Egr-1.更多还原