首都医科大学学报 ›› 2005, Vol. 26 ›› Issue (1): 48-50.

• 论著·基础研究 • 上一篇    下一篇

PD98059对11,12-EET及缺血预处置大鼠心功能保护作用的影响

王红霞, 曾翔俊, 闫丽, 芦玲巧, 张立克   

  1. 首都医科大学病理生理学教研室
  • 收稿日期:2004-09-10 修回日期:1900-01-01 出版日期:2005-02-24 发布日期:2005-02-24
  • 通讯作者: 张立克

PD98059 on Heart Function Endured 11,12-EET and Ischemia Preconditioning

Wang Hongxia, Zeng Xiangjun, Yan Li, Lu Lingqiao, Zhang Like   

  1. Department of Pathophysiology, Capital University of Medical Sciences
  • Received:2004-09-10 Revised:1900-01-01 Online:2005-02-24 Published:2005-02-24

摘要:

为观察PD98059对给予11, 12-EET或缺血预处置在体大鼠再灌注心功能的影响, 了解磷酸化ERK1/ERK2的表达在上述心脏保护中的作用, 使用雄性Wistar大鼠, 通过结扎(60min)和松开(30min)冠状动脉左前降支, 复制缺血/再灌注模型;采用缺血5min, 再灌注5min 2次造成缺血预处置;6.24×10-8mol/L 11, 12-EET通过静脉给予。计算机记录再灌注过程中心功能的变化;实验结束时取心肌采用WesternBlot法测定ERK1/ERK2的表达。结果显示:再灌注30min, I/R组的+dp/dtmax(收缩期左心室内压上升的最大变化速率)、-dp/dtmax(舒张期左心室内压下降的最大变化速率)和LVDP(左心室发展压)均显著低于SI+I/R组和EET+I/R组(P<0.05);SI+I/R+PD组的+dp/dtmax、-dp/dtmax及LVDP均明显低于SI+I/R组(P<0.05), EET+I/R+PD组的+dp/dtmax、-dp/dtmax及LVDP明显低于EET+I/R组(P<0.05)。研究表明:6.24×10-8mol/L11, 12EET及缺血预处置均有保护心功能的作用;这种保护作用通过激活缺血/再灌注时ERK1/ERK2的表达而实现。

Abstract:

The aim was to investigate the effect of PD98059 on heart function endured 11, 12-EET a nd ischemia preconditioning and know about the effect of the expression of phosp horylated ERK1/ERK2 on the cardiac protection. Adopting ligating 60 min a nd releasing 30 min to make a ischemic/reperfusion model; ligating 5 min and rel ea sing 5 min (two times) to replicate ischemic preconditioning model. Observing th e changing of heart function during reperfusion process and detecting the expressi on of ERK1/ERK2 through western blot method. There was significant di fferen ce contrasting the heart function I/R group with SI+I/R and EET+I/R group, and t he heart function was significantly decreased after PD98059 infusion. The phosph orylated expression of ERK of I/R group was significantly lower than SI+I/R and E ET+I/R group, and the phosphorylated expression of ERK was significantly decreas ed after PD98059 infusion. It suggests that 6.24×10-8 mol/L 11,12-EET h as the effect of protecting myocardium function that is inducted by increasing the expression of phosphorylated ERK1/ERK2.

Key words: 11, 12-epoxyeicosatrienoic acid, is chemia-reperfusion injury, ischemic preconditioning, excellular signal regulated kinase

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