全脑缺血再灌注损伤中JNK及Bim蛋白的表达

被引：14

作者：

陈宏志

陈卫民

机构：

[1] 中国医科大学附属盛京医院麻醉科

来源：

中国现代医学杂志 | 2007年 / 07期

关键词：

全脑缺血再灌注损伤; 凋亡; p-JNK; Bim;

D O I：

暂无

中图分类号：

R363 [病理生理学];

学科分类号：

100104 ;

摘要：

目的探讨大鼠全脑缺血再灌注氨基末端激酶或应激活化激酶(p-JNK)及与Bcl-2相互作用的细胞死亡调解子(Bim)蛋白表达的变化。方法构建大鼠全脑缺血再灌注模型,采用TUNEL法原位检测凋亡锥体细胞,免疫印迹检测不同实验组中Bim及p-JNK蛋白表达。结果缺血再灌注各组神经元细胞的凋亡率明显高于假手术组(P<0.05)。缺血再灌注组p-JNK及Bim蛋白表达积分光密度值与假手术组相比差异有显著性(P<0.05)。结论在脑缺血及在灌注损伤中存在有JNK途径的过度激活,p-JNK蛋白与Bim蛋白表达为正相关。JNK途径的激活导致Bim蛋白表达增加,进而导致神经元细胞的凋亡明显增加。

引用

页码：809 / 812

页数：4

共 12 条

[1]

Bcl-2in hibits death of central nervos cell in duced by multi pleagents. ZHANG L,SARAFIAN T,KANE D,et al. Proceedings of the National Academy of Sciences of the United States of America . 1993

[2]

Neuron[P]. KUTKOVETSKYI VALENTYN YAKOVYCH;TURTI MARYNA VALENTYNIVNA.UA106289U,2016-04-25

[3]

Expression of TNF-αand ICAM after focal cerebral ischemia in IL-βcon-verting enzyme deficient mice. YANG GY,SCHIELKE GP,GONG C,et al. Journal of Cerebral Blood Flow and Metabolism . 1999

[4]

Neuroprotective effect of VEGF on middle cerebr alartery occlusion rat. MAN SM,CUI J,WANG L,et al. China Journal of Chinese Materia Medica . 2005

[5]

Delayed neuronal cell death in the rat hippocampusis medited by the mitogen-activat-ed protein kinases ignal transduction pathway. OZAWA H,SHIODA S,DOHI K,et al. Neuro Sci Let-ters . 1999

[6]

BH3-only proteins-evolutionarily conserved pro-apoptotic Bcl-2family members essential for initi-ating programmed cell death. BOUILLET P,STRASSER A. Journal of Cell Science . 2002

[7]

Lasting Nterminal phosphorylation of c-Jun and activation of c-Jun N-terminal kinases after neuronal injury. HERDEGEN T,CLARET FX,KALLUNKI T,et al. Neuroscience . 1998

[8]

Mitogen activated protein kinasecas cadesas regulator-sof stress responses. KARIN M. Annals of the New York Academy of Sciences . 1998

[9]

The JNK signaling transduction pathway. CLAIRE R,ROGER J. Current Opinion . 2002

[10]

Quick guide Jnk. WEITZMAN JB. Current Biology . 2000

← 1 2 →