大鼠脑创伤后ERK信号转导通路对神经细胞凋亡的影响  

Influences on ERK signal transduction pathways to nerve cell apoptosis in rats after trauma

作　　者：路文婷[1] 陈朝旺[2] 高俊玲[3] 

机构地区：[1]河北省邯郸市第一医院中西医结合科,河北邯郸056000 [2]河北省邯郸市第一医院急诊内科,河北邯郸056000 [3]华北煤炭医学院组胚教研室,河北唐山063000

出　　处：《中国医药导报》2012年第18期39-41,共3页China Medical Herald

基　　金：河北省科技领军人才基金项目(项目编号:06547008D-7)

摘　　要：目的探讨细胞外调节激酶(ERK)信号转导机制对大鼠脑创伤后神经细胞凋亡的作用。方法建立重型弥漫性脑损伤(TMI)模型,70只雄性SD大鼠分为创伤组和对照组,其中创伤组分为伤后10、30 min、3、6、24、48、72 h 7个时相点,采用免疫组化法检测细胞凋亡相关基因ERK、caspase-3的表达,原位末端标记(TUNEL)法检测细胞凋亡。结果创伤组海马CA1区P-ERK1/2和caspase-3蛋白表达在伤后3 h较对照组显著升高(P<0.05),伤后6 h达高峰(P<0.01),后逐渐下降,P-ERK1/2在伤后24 h表达量仍明显高于对照组(P<0.05),caspase-3在伤后72 h仍有大量表达;镜下对照组未见TUNEL阳性细胞,创伤组在伤后3 h凋亡细胞数明显增多,伤后48 h达高峰,均显著高于对照组(P<0.01)。结论大鼠脑创伤后ERK信号转导通路激活,可能通过诱导caspase-3蛋白表达,进而导致神经细胞凋亡。Objective To study the mechanism of ERK signal transduction pathways to nerve cell apoptosis in rats after trauma. Methods Heavy diffuse brain injury （TMI） model was established. Male SD rats （n = 70） were randomly divided into two groups： trauma group and control group. Tuma group was divided into 7 subgroups according to time phase follow- ing brain injury： 10, 30 min, 3, 6, 24, 48, 72 h. The expression of p-ERK1/2 and caspase-3 were detected by immunity histochemistry staining; the apoptosis of nerve cell was detected by TUNEL. Results The expression of p-ERK1/2, cas- pase-3 in the hippocampasl CA1 area in TBI group were increased significantly after injury 3 h compared to those in the control group （P 〈 0.05）, and reached the peak at 6 h（ P 〈 0.01）, the overexpression of p-ERK1/2 and caspase-3 contin- ued to 24 h and 72 h respectively; TUNEL positive cells were increased in TBI group from 3 h to 72 h, and reach the peak at 48 h （P 〈 0.01）. Conclusion The activation of ERK signal transduction pathway and expression of caspase-3 may is one of mechanisms of nerve cell apoptosis following traumatic brain iniurv in rats.

关 键 词：大鼠 脑创伤 蛋白激酶类 细胞凋亡 

分 类 号：R651.15[医药卫生—外科学]