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中国临床药理学与治疗学 ›› 2004, Vol. 9 ›› Issue (12): 1343-1348.

• 研究原著 • 上一篇    下一篇

碘化N-正丁基氟哌啶醇对Egr-1 转录及表达的影响

唐昭, 石刚刚, 张艳美, 尹俊, 周燕琼, 黄展勤, 高分飞   

  1. 汕头大学医学院药物研究室, 汕头 515041, 广东
  • 收稿日期:2004-10-21 修回日期:2004-12-09 出版日期:2004-12-26 发布日期:2020-11-19
  • 通讯作者: 石刚刚, 男, 教授, 博士生导师, 研究方向:心血管新药研究与开发。Tel:0754-8900301 E-mail:ggshi@stu.edu.cn
  • 作者简介:唐昭, 男, 硕士生。Tel:0754-8900432 E-mail:gztang@stu.edu.cn
  • 基金资助:
    国家自然科学基金项目(No30472028);广东省科技计划项目(NoC30104);广东省自然科学基金重点项目(No021235)

Effects of N-n-butyl haloperidol iodide (F2) on Egr-1 mRNA and protein expression after myocardial ischemia-reperfusion

TANG Zhao, SHI Gang-Gang, ZHANG Yan-Mei, YIN Jun, ZHOU Yan-Qiong, HUANG Zhan-Qin, GAO Fen-Fei   

  1. Department of Drug Institute, Medical College, Shantou University, Shantou 515041, Guangdong, China
  • Received:2004-10-21 Revised:2004-12-09 Online:2004-12-26 Published:2020-11-19

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-butyl haloperidol iodide,F2) 对早期生长反应蛋白-1(early growth response-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5 min, 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-1 mRNA 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。

关键词: 碘化N-正丁基氟哌啶醇, Egr-1, 心肌, 缺血再灌注损伤, 血流动力学, 炎性损伤, 中性粒细胞, 转录因子

Abstract: AIM: To investigate the effects of N-nbutyl haloperidol iodide (F2) on Egr-1 mRNA and protein expression in the model of rats with myocardial ischemiareperfusion. METHODS: The myocardial ischemiareperfusion injury animal model was established by occluding rat's left anterior descending branch of coronary artery for 60min and later opening the ligation to reperfusion for 180 min in vivo.F2 were administered by intravenous injection before the onset of ischemia for 5 min.The changes of hemodynamics were recorded during the experiment, and then the ischemia tissue was extract.The inflammation was observed by tissue section.The Egr-1 gene transcription and protein expression were detected by RT-PCR and Western-blot, respectively.RESULTS: F2 reduced the levels of Egr-1 mRNA and protein, relieve inflammation and ameliorate the hemodynamics of ischemia-reperfusion injured myocardium.CONCLUSION: F2 can relieve inflammatory injury and protect myocardial function in rats with myocardial ischemia-reperfusion, and the mechanism may be related to attenuating the transcription and expression of Egr-1.

Key words: N-n-butyl haloperidol iodide, Egr-1, myocardial ischemia-reperfusion injury, hemodynamics, inflammation, neutrophil, transcription factor

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