全脑缺血再灌注损伤中JNK及Bim蛋白的表达  

Expression of jenes Bim and JNK signaling transduction pathway in rat brain follwing cerebral ischemia

作　　者：陈宏志[1] 陈卫民[1] 

机构地区：[1]中国医科大学附属盛京医院麻醉科,辽宁沈阳110004

出　　处：《中国现代医学杂志》2007年第7期809-812,共4页China Journal of Modern Medicine

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。[Objective] To study the JNK pathway and its relationship with Bim in cerebral ischemia reperfusion lesion. [Methods] To construct the model of rat cerebral ischemia reperfusion lesion, collect the tissues of dentate gyrus of rats and make coronal sections, observe the number of apoptosis cells in hippocampus under light microscope. To examine the apoptotic pyramidal neuron by TUNEL test and the expression of Bim and p-JNK in different groups by immuno- blotting test. [Results] The apoptosis rate and the necrosis rate in ischemia reperfusion groups are significantly higher than that of control （P 〈0.05）, The expression of p-JNK in ischemia reperfusion groups was different to that of control （P 〈0.05）, peaked in 12 h, then decreased gradually. The expression of Bim in ischemia reperfusion groups was different to that of control （P 〈0.05）, and increased with the elongation of the time of reperfusion, peaked in 2 h, then decreased gradually. [Conclusions] The JNK pathway was overactivated during the cerebral ischemia and the reperfusion lesion, the expression of p-JNK was increased. The expression of p-JNK was positively related to that of Bim, which is to say that, the activation of JNK pathway resulted in the increase of Bim expression. The expression of p-JNK was positively related to that of Bim, which is to say that, the activation of JNK pathway resulted in the increase of Bim expression.

关 键 词：全脑缺血再灌注损伤 凋亡 P-JNK BIM 

分 类 号：R-332[医药卫生]