抑制ERK1/2对大鼠弥漫性脑损伤后细胞凋亡的影响  

Effects of inhibition of ERK1/2 on cell apoptosis in rats with diffuse brain injury

作　　者：李金星 赵海梅[2] 姜晓兵[3] LI Jin-xing;ZHAO Hai-mei;JIANG Xiao-bing(Department of Neurosurgery, Chinese Traditional Medicine Hospital Of Shenzhen City, Shenzhen 518033, China)

机构地区：[1]深圳市中医院神经外科,广东518033 [2]南昌大学第三附属医院老年医学科,南昌330008 [3]华中科技大学同济医学院附属协和医院神经外科,武汉430022

出　　处：《中国临床神经外科杂志》2019年第1期39-41,共3页Chinese Journal of Clinical Neurosurgery

摘　　要：目的探讨抑制细胞外信号调节激酶1/2(ERK1/2)对大鼠弥漫性脑损伤(DBI)后脑组织细胞凋亡的影响。方法按随机数字表法将228只成年SD大鼠随机分为假手术组(n=12)、DBI组(n=72)、阻滞剂组(n=72)、对照组(n=72),后三组按动物处死时间分为30 min、3 h、24 h、48 h、72 h和7 d六个亚组,每亚组12只。参照Mamarou自由落体方法制作重型DBI模型。阻滞剂组损伤后尾静脉注射ERK1/2特异性阻滞剂U0126(0.05 mg/kg),对照组注射等量溶剂二甲基亚砜。免疫印迹法法检测脑组织磷酸化ERK1/2(p ERK1/2)的表达水平,免疫组化法检测Caspase-3表达,流式细胞术检测细胞凋亡率。结果伤后30 min,脑组织pERK1/2表达水平显著增高(P<0.05),并持续高水平表达至72 h,伤后7 d与假手术组无统计学差异(P>0.05)。伤后3 h,脑组织Caspase-3表达水平和细胞凋亡率均明显增高,72 h达到高峰,伤后7 d仍明显高于假手术组(P<0.05)。伤后30 min、3 h、24 h、48 h、72 h和7 d,阻滞剂组脑组织Caspase-3表达水平和细胞凋亡率均明显低于DBI组和对照组(P<0.05),而DBI组和对照组均无统计学差异(P>0.05)。结论阻滞ERK1/2通路,可显著抑制DBI大鼠脑组织Caspase-3的表达,降低细胞凋亡率。Objective To study the effect of inhibition of extracellular signal regulated kinase1/2 (ERK1/2) on cell apoptosis in the cerebral tissues of the rats with diffuse brain injury (DBI). Methods Two hundred and twenty-eight SD rats were randomly divided into sham operation (n=12), DBI (n=72), experimental (n=72) and control (n=72) groups. Severe rats DBI models were established by Mamarou's free falling-body method in DBI, experimental and control groups. U0126, a special inhibitor of ERK1/2, was injected respectively into the tail veins of rats immediately after DBI in the experimental and control groups. Phosphorylated ERK1/2 (pERK1/2) and caspase-3 expression in the cerebral tissues were determined respectively by Western blotting and immunohistochemical staining. The cell apoptosis rate in the cerebral tissues was detected by flow cytometry method. Results The levels of pERK1/2 expression were significantly higher in DBI and control groups than those in the experimental group (P<0.01), which were significantly higher than that in the sham operation group (P<0.01) 0.5, 3, 24, 48 and 72 hours after DBI. The levels of Caspase-3 expression in the cerebral tissues were significantly higher in DBI and control groups than those in the experimental group (P<0.05), which were significantly higher than those in the sham operation group (P<0.05) 3, 24, 48, 72 and 168 hours after DBI. The rats of cell apoptosis in the cerebral tissues were significantly higher in the DBI and control groups than those in the experimental group (P<0.05), which were significantly higher than that in the sham operation group (P<0.05) 3, 24, 48 72 and 168 hours after DBI group. Conclusion The inhibition the activation of ERK1/2 can decrease expression of Caspase-3 and cell apoptosis in the brain tissue of the rats with DBI.

关 键 词：弥漫性脑损伤 ERK1/2 CASPASE-3 细胞凋亡 大鼠 

分 类 号：R651.15[医药卫生—外科学]