缺血后处理对短暂性脑缺血后蛋白质氧化损伤的影响  

The effects of ischemic postconditioning on protein oxidation induced by transie nt ischemia

作　　者：孟繁凯[1] 李再雨[2] 徐宁[2] 杨福伟[2] 李光民[1] 罗毅男[2] 葛鹏飞[2] 

机构地区：[1]吉林省人民医院神经外科,吉林长春130021 [2]吉林大学白求恩第一医院神经外科

出　　处：《中国老年学杂志》2012年第15期3221-3223,共3页Chinese Journal of Gerontology

基　　金：国家自然科学基金面上项目(No.30973110);教育部直属高校自然科学基本科研业务费项目(No.421030863428);吉林省科技厅项目(No.20080139)

摘　　要：目的探讨后处理对短暂性脑缺血后脑损伤及氧化应激性蛋白质损伤的影响。方法大鼠MCAO局灶脑缺血再灌注模型,分为假手术组,缺血组及后处理组。缺血后处理方法为缺血结束后恢复脑血流30 s再阻断30 s为1个循环,共3个循环。采用TTC染色计算梗死脑组织的体积。差速离心法分离线粒体。荧光测定法检测线粒体内过氧化氢含量。分光光度计法检测蛋白质氧化产物羰基化合物含量。结果缺血后处理显著降低了局灶脑缺血后脑梗死的体积;线粒体内过氧化氢的含量显著降低;蛋白质氧化产物羰基化合物的含量显著降低。结论缺血后处理能够通过降低氧化应激性蛋白质损伤保护缺血再灌注所致的脑损伤。Objective To investigate the effects of ischemic post-conditioning on brain injury induced by transient ischemia and reperfusion and protein damage due to oxidative stress. Methods Transient ischemia and reperfusion was established by rat middle cerebral artery occlusion（MCAO） model. All the rats were divided into sham-operated, ischemia and ischemic post-conditioning groups. Ischemic post-conditioning rats were subjected to 3 cycles of 30 s/30 s reperfusion/re-occlusion after 2 h of ischemia. The volume of the infarct brain was measured by Trc. Mitochondria was isolated via differential centrifuge. F]uoremetry was used to assay the content of hydrogen dioxides. Spectrophotometer was used to measure the quantity of the products of protein oxidization. Results The infarct volume of the damaged brain was caused by transient ischemia, the content of hydrogen dioxide and carboxyl products of protein oxidation were all decreased significantly by ischemic post-conditioning. Conclusions Ischemic post-conditioning prote.cts the damaged brain tissue caused by transient ischemia via reducing oxidative stress induced protein oxidation.

关 键 词：缺血后处理 氧化应激反应 蛋白质氧化 短暂性脑缺血 

分 类 号：R-33[医药卫生]