阻滞弥漫性脑损伤ERK1/2信号通路对星形胶质细胞反应的作用  

Effect of ERK1/2 Activation Inhibition on Reactive Astrogliosis in Rats with Traumatic Diffuse Brain Injuries

作　　者：李金星[1] 赵海梅[1] 李玉[2] 王翀[2] 赵甲山[2] 朱贤立[2] 

机构地区：[1]南昌市第一医院神经外科,江西南昌330008 [2]华中科技大学同济医学院附属协和医院神经外科,湖北武汉430022

出　　处：《中国临床神经外科杂志》2007年第8期480-483,共4页Chinese Journal of Clinical Neurosurgery

摘　　要：目的研究阻滞弥漫性脑损伤急性期ERK1/2信号通路过度激活对星形胶质细胞反应的影响。方法制作大鼠外伤性弥漫性脑损伤模型,打击损伤前30min自尾静脉注射U0126。Western blot法检测损伤脑皮层pERK1/2表达水平,免疫组化染色法检测pERK1/2和GFAP在损伤脑组织中的表达。结果pERK1/2表达在损伤后迅速、显著升高,5min为表达高峰,其后下降,但直到损伤后72h都有高水平表达,至7d下降至基础水平。损伤后各个时间点,U0126组pERK1/2水平较DBI组明显降低(P<0.05)。U0126组与DBI组比较,12～72h各时间点GFAP阳性细胞平均光密度值降低(P<0.05)。结论弥漫性脑损伤诱导了强烈的ERK1/2信号通路激活和星形胶质细胞反应,U0126能够剂量依赖性抑制GFAP的表达,抑制急性期星形胶质细胞反应。Objective To explore the effect of ERK1/2 activation inhibiton on reactive astrogliosis in rats with acute traumatic diffuse brain injuries （DBI）. Methods DBI model was established by Marmarou＇s free falling-body method. U0126 was injected intravenously 30 minute before DBI. Western blot analysis and immunohistochemistry were used to detect the expression level and regional distribution of phospho-ERK1/2（pERK1/2） in the injured brain tissue respectively. Immunohistochemistry was used to evaluate the expression of glial fibril acidic protein （GFAP）. Results The expression level of pERK1/2 significantly increased and peaked 5 minute after DBI, and still was significantly higher than that in the sham group up to 72 hours after DBI （P〈0.01）. The expression level of pERK1/2 was significantly lower in U0126 treatment group than that in DBI control group from 5 min to 72 hours after DBI （P〈0.01 or P〈0.05）. The optic density of positive GFAP cells in U0126 treatment group was significantly lower than that in the DBI control group from 12 to 72 hours after DBI （P〈0.05）. Conclusions The DBI can intensely induce ERK1/2 pathway activation and reactive astrogliosis, which can be attenuated by inhibition of ERK1/2 pathway.

关 键 词：弥漫性脑损伤:细胞外信号调节激酶:胶质纤维酸性蛋白 

分 类 号：Q786[生物学—分子生物学] R651.15[医药卫生—外科学]