Epoxyeicosatrienoic acids(EETs)are the metabolic products of arachidonic acid(AA). They have the function of stimulating cell division, inhibiting platelet aggregation and regulating the transfer of cell calcium. In r...Epoxyeicosatrienoic acids(EETs)are the metabolic products of arachidonic acid(AA). They have the function of stimulating cell division, inhibiting platelet aggregation and regulating the transfer of cell calcium. In recent years, more and more people paid their attention to the effects of EETs on heart. This article will give a review about EETs and the relationship between EETs and heart.展开更多
目的:观察11,12-EET延迟性保护作用对缺血再灌注大鼠心肌ERK活性及磷酸化ERK表达的影响,探讨其在11,12-EET延迟性保护中的作用。方法:复制大鼠心肌缺血/再灌注模型;观察缺血/再灌注期间心脏收缩期左心室内压上升的最大变化速率(+dp/dtm ...目的:观察11,12-EET延迟性保护作用对缺血再灌注大鼠心肌ERK活性及磷酸化ERK表达的影响,探讨其在11,12-EET延迟性保护中的作用。方法:复制大鼠心肌缺血/再灌注模型;观察缺血/再灌注期间心脏收缩期左心室内压上升的最大变化速率(+dp/dtm ax)及舒张期左心室内压下降的最大变化速率(-dp/dtm ax);采用免疫共沉淀法测定大鼠心肌组织中细胞外调节激酶(ERK)的活性,采用W estern b lotting法测定大鼠心肌组织中磷酸化ERK的表达。结果:I/R组缺血60 m in及再灌注30 m in两个时段±dp/dtm ax均低于sham组(P<0.05),24 hE-ET+I/R组缺血60 m in及再灌注30 m in两个时段±dp/dtm ax明显高于I/R组(P<0.05),而24hEET+PD+I/R组缺血60 m in及再灌注30 m in两个时段±dp/dtm ax明显低于24hEET+I/R组(P<0.05)。ERK的活性24hEET+I/R高于norm al组,24hEET+I/R组低于24hEET+PD+I/R组。磷酸化ERK的表达I/R组高于norm al组和sham组,24hEET+I/R高于I/R组,24 hEET+I/R组低于24hEET+PD+I/R组。结论:外源性11,12-EET具有延迟性心脏保护作用,大量激活磷酸化的ERK参与这种保护作用。展开更多
文摘Epoxyeicosatrienoic acids(EETs)are the metabolic products of arachidonic acid(AA). They have the function of stimulating cell division, inhibiting platelet aggregation and regulating the transfer of cell calcium. In recent years, more and more people paid their attention to the effects of EETs on heart. This article will give a review about EETs and the relationship between EETs and heart.
文摘目的:观察11,12-EET延迟性保护作用对缺血再灌注大鼠心肌ERK活性及磷酸化ERK表达的影响,探讨其在11,12-EET延迟性保护中的作用。方法:复制大鼠心肌缺血/再灌注模型;观察缺血/再灌注期间心脏收缩期左心室内压上升的最大变化速率(+dp/dtm ax)及舒张期左心室内压下降的最大变化速率(-dp/dtm ax);采用免疫共沉淀法测定大鼠心肌组织中细胞外调节激酶(ERK)的活性,采用W estern b lotting法测定大鼠心肌组织中磷酸化ERK的表达。结果:I/R组缺血60 m in及再灌注30 m in两个时段±dp/dtm ax均低于sham组(P<0.05),24 hE-ET+I/R组缺血60 m in及再灌注30 m in两个时段±dp/dtm ax明显高于I/R组(P<0.05),而24hEET+PD+I/R组缺血60 m in及再灌注30 m in两个时段±dp/dtm ax明显低于24hEET+I/R组(P<0.05)。ERK的活性24hEET+I/R高于norm al组,24hEET+I/R组低于24hEET+PD+I/R组。磷酸化ERK的表达I/R组高于norm al组和sham组,24hEET+I/R高于I/R组,24 hEET+I/R组低于24hEET+PD+I/R组。结论:外源性11,12-EET具有延迟性心脏保护作用,大量激活磷酸化的ERK参与这种保护作用。
