大鼠脑创伤后ERK通路对皮质神经细胞c-fos蛋白表达及凋亡的影响  

Influence of ERK on Nerve Cell Apoptosis of Cortex Following Traumatic Brain Injury in Rats

作　　者：高俊玲[1] 田艳霞[1] 陈万欣[2] 张志民[3] 

机构地区：[1]华北煤炭医学院组织胚胎学教研室,唐山063000 [2]承德医学院附属医院肾脏内科 [3]承德医学院附属医院心脏外科

出　　处：《天津医药》2008年第1期46-48,82,共4页Tianjin Medical Journal

基　　金：河北省科技领军人才基金,博士基金(基金编号:06547008D-7);中国人事部留学人员优秀科技项目资助基金(项目编号:2007-17)

摘　　要：目的:探讨细胞外调节激酶(ERK)信号转导机制在颅脑创伤中的作用。方法:建立大鼠重型弥漫性颅脑创伤(TBI)模型,92只雄性SD大鼠分为创伤组和对照组,其中创伤组又分为伤后10min、30min、3h、6h、24h、48h和72h7个时相组,采用免疫组化、蛋白印迹方法分别定性、定量检测以上两组ERK的表达,用免疫组化法检测c-fos蛋白表达,用原位末端标记法检测凋亡细胞。结果:创伤组p-ERK1/2和c-fos的表达及TUNEL阳性细胞在不同时间大多高于对照组:创伤组p-ERK1/2蛋白表达在伤后10min已较对照组明显升高(P<0.05),伤后6h达高峰,24h仍有大量表达,仍明显高于对照组(P<0.01),至伤后48h降至对照组水平(P>0.05);创伤组c-fos免疫反应性在伤后10min开始升高(P<0.01),伤后6h达高峰(P<0.01),48h以后明显减弱,但仍高于对照组(P<0.01);镜下对照组未见TUNEL阳性细胞,创伤组伤后3h偶见TUNEL阳性细胞,6h明显增多,48h达高峰,均显著高于对照组(P<0.01)。结论:大鼠脑创伤后ERK通路过度激活,可能通过诱导c-fos蛋白表达,进而导致神经细胞凋亡。Objective： To investigate the effect of extracellular-signal regulated protein kinase （ERK） signal transduction mechanism in traumatic brain injury （TBI） in rats. Methods： The rat model of TBI was made according to the method of Marmarou （1994）. A total of 92 male Sprague-Dawley rats were randomly divided into control and TBI groups. The rats in group of TBI were divided into 7 subgroups according to the time phase after brain injury,which were 10 min,30 min, 3 h, 6 h, 24 h, 48 h and 72 h. The expression of ERK was detected by immunohistochemical and Western blot methods. The expression of c-fos was detected by immunohistochemical method. The apoptosis of cortex cell was detected by TUNEL. Results： The activities of p-ERK1/2, c-fos and TUNEL positive cells were increased in TBI group compared to those in the control group. Conclusion： The excessive activation of ERK is one of mechanisms of nerve cell apoptosis by inducing c-fos protein following traumatic brain injury in rats.

关 键 词：大鼠 创伤和损伤 蛋白激酶类 颅脑损伤 细胞凋亡 

分 类 号：R445.1[医药卫生—影像医学与核医学] R743.3[医药卫生—诊断学]