映山红总黄酮对脑缺血大鼠ERK通路的影响  

Effect of Total Flavones of Rhododendra simsii on the Activation of ERK Induced by Cerebral Ischemia-reperfusion in Rats

作　　者：郭岩[1] 陈志武[1] 

机构地区：[1]安徽医科大学药理学教研室,安徽合肥230032

出　　处：《中药材》2012年第7期1108-1111,共4页Journal of Chinese Medicinal Materials

基　　金：安徽医科大学博士科研资助项目(XJ200814)

摘　　要：目的:观察映山红总黄酮(TFR)对大鼠全脑缺血-再灌注损伤是否具有保护作用,以及保护作用是否与ERK信号转导通路有关。方法:采用四血管结扎法建立大鼠全脑缺血-再灌注损伤模型。记录脑缺血前、缺血10min和再灌注后5、10、15、30、45、60 min的脑电图改变;采用蛋白免疫印迹方法,测定大鼠脑皮质和海马组织中ERK1/2和p-ERK1/2在脑缺血-再灌注后表达的变化,以及TFR对此变化的影响。结果:脑缺血时大鼠的脑电图幅度迅速下降,再灌注后脑电幅度逐渐恢复。再灌注45 min和60 min时,映山红总黄酮各剂量组脑电图幅度与模型组比较差异显著(P<0.05或P<0.01)。蛋白印迹结果显示,与模型组比较,映山红总黄酮各剂量组p-ERK1/2的表达显著性升高(P<0.05)。结论:TFR对大鼠全脑缺血-再灌注损伤有保护作用,其机制可能与增加大鼠脑组织中ERK1/2的激活有关。Objective：To study the effect of total flavones of Rhododendron simsii（TFR）on the activation of ERK induced by cerebral ischemia-reperfusion in rats and its possible mechanism.Methods： Cerebral ischemia-reperfusion were induced by 4-vessel occlusion in rats.Changes in electroencephalogram were recorded before and 10min after ischemia and 5,10,15,30,45 and 60 min after reperfusion.The activation of ERK1/2 and p-ERK1/2 of cerebral cortex and hippocampus was investigated by western blot.Results：Compared with sham-operate group,EEG amplitude decreased significantly after ischemia and recovered after reperfusion in NS control and at 45 min and 60 min,EEG amplitude of TFR（15,30,60 mg/kg） groups was significantly higher than that of NS control（P〈0.05 or P〈0.01）.TFR（30,60 mg/kg） could increase the activation of ERK1/2 after cerebral ischmia-reperfusion.Conclusion：TFR（15,30,60 mg/kg） could significantly promote the recovery of EEG and the mechanism might be associated with the increase of the activation of ERK1/2 after cerebral ischemia-reperfusion.

关 键 词：映山红总黄酮 脑缺血-再灌注 脑电图 胞外信号调节激酶 

分 类 号：R285.5[医药卫生—中药学]