摘要
目的:观察大鼠局灶性脑缺血再灌注模型磷酸化c-Jun氨基末端激酶(p-JNK)和蛋白丝裂原活化蛋白激酶磷酸酶1(MKP-1)的变化,探索p-JNK和MKP-1在脑缺血再灌注损伤中的作用。方法:雄性Wistar大鼠,随机分成假手术组,缺血2 h再灌注4 h、24 h、48 h和72 h组。应用"线栓法"实现大鼠右侧大脑中动脉闭塞,2 h后拔出线栓进行再灌注,并在相应时间点处死大鼠。利用免疫组化法观察p-JNK和MKP-1蛋白表达水平的变化。结果:与假手术组相比,缺血再灌注组大鼠梗死灶周围区皮质p-JNK和MKP-1蛋白表达水平明显升高(P<0.05),开始于再灌注后4,48 h达到高峰,72 h开始下降。结论:p-JNK和MKP-1相互作用,参与了脑缺血再灌注损伤的形成。
Aim： To observe the expressions of phosphorylation of c-Jun amino-terminal kinases（p-JNK） and mitogen activated protein kinase phosphatase-1 （MKP-1） in rats with focal brain ischemia-reperfusion and clarify the effects of p-JNK and MKP-1 in brain ischemia-reperfusion injury. Methods： Male Wistar rats were randomly divided into sham-operated group and ischemia-reperfusion groups. The model of focal brain ischemia- reperfusion injury was induced by middle cerebral artery occlusion. After 2 hours of ischemia and 4, 24, 48 and 72 hours of reperfusion, the animals were sacrificed. Immunohistochemistry was used to detect the levels of p-JNK and MKP-1 protein expressions. Results： Compared with sham-operated group, ischemia- repel＇fusion significantly increased the expressions of p-JNK and MKP-1 in the peri-infarct cortex surrounding the primary infarct which began at 4 hours after reperfusion （P〈0.05）, peaked at 48 hours and subsided at 72 hours. Condusion： This study indicates that p-JNK and MKP-1 react with each other during the course of focal brain ischemia-reperfusion and both of them take part in the mechanism of ischemia-reperfusion injury.
出处
《中国临床神经科学》
2010年第2期126-129,共4页
Chinese Journal of Clinical Neurosciences
基金
黑龙江省卫生厅科研课题(编号:2007-216)
哈尔滨医科大学2009年创新基地项目
