ERK1/2信号传导通路在大鼠局灶性急性脑缺血再灌注中的作用  

The Effect of ERK1 /2 Signal Transduction Pathway in Rats Focal Acute Ischemia-reper-fusion

作　　者：杨洋[1] 刘晓楠[1] 马超[1] 姜源[1] 孙晓红[1] 

机构地区：[1]中国医科大学附属第四医院神经内科,辽宁省沈阳市110032

出　　处：《中国动脉硬化杂志》2013年第11期987-992,共6页Chinese Journal of Arteriosclerosis

摘　　要：目的研究ERK1/2信号传导通路在局灶性急性脑缺血再灌注中的作用。方法健康雄性SD大鼠,随机分为假手术组和缺血组,缺血组又分为脑缺血再灌注6、12、24、48和72 h组,每组6只,共计36只。采用线栓法建立大脑中动脉闭塞(MCAO)模型。应用免疫组织化学方法测定CD34、血管生成素2(Ang-2)、细胞外信号调节激酶1/2(ERK1/2)蛋白表达。结果 Ang-2及ERK1/2在局灶性脑缺血再灌注大鼠模型中均在24 h达到高峰。结论 ERK1/2信号传导通路参与了血管生成素对新生血管的促进作用。Aim This paper studies the effect of ERK1/2 signal transduction in focal acute brain ischemia-reper- fusion. Methods 36 healthy male SD rats were randomly divided into sham operation group and ischemia group. Is- chemia group was further divided into brain ischemia-reperfusion with differernt time （6, 12, 24, 48 and 72 h）. Suture- occluded method was used to build cerebral middle artery infarction model （MCAO）. CD34, Ang-2 and ERKI/2 were detected through immunohistochemical method. Results Ang-2 and ERK1/2 in focal cerebral ischemia-reperfusion rat model had dynamic change, and both reached peak at 24 hour. Conclusion ERK1/2 signal transduction way takes part in the promotion effect of angiogenesis of angiopoietin.

关 键 词：ERK 脑缺血再灌注 血管生成素 

分 类 号：R363[医药卫生—病理学]