血红素氧合酶-2基因缺失对氧化应激性脑损伤的保护作用(英文)  

Protective role of heme oxygenase-2 gene deletion in oxidative stress-induced brain injury

作　　者：屈延[1] 章翔[1] 陈晶[1] 马新[1] Raymond F.Regan 

机构地区：[1]第四军医大学西京医院神经外科 [2]Department of Emergency Medicine, Thomas Jefferson University, 1020 Sansom Street, Thompson Building Room 239, Philadelphia, PA 19107, USA

出　　处：《中华神经外科疾病研究杂志》2005年第3期197-203,共7页Chinese Journal of Neurosurgical Disease Research

基　　金：SupportedbytheNationalNaturalScienceFoundationofChina(30270534)

摘　　要：目的探讨血红素氧合酶2基因缺失对血红素诱导氧化应激性脑损伤的保护作用。方法分别将6μl(8μmol/L)灭菌氯高铁血红素定向注入野生型小鼠和基因(HO2)敲除小鼠的纹状体内,72h后分别检测纹状体细胞生存率,蛋白和脂类的氧化作用。用蛋白质印迹法检测血红素氧合酶1,2(HO1)的表达。结果与野生型相比,基因(HO2)敲除小鼠纹状体内蛋白和脂类的氧化作用显著降低,而纹状体细胞的存活率显著增加;HO1的表达在两种小鼠注射前后没有明显差异。结论结果提示,血红素氧合酶2基因缺失对血红素诱导的氧化应激性脑损伤具有保护作用;选择性抑制神经元血红素氧合酶2基因的表达可减轻氧化应激性脑损伤。Objective To investgate heme oxygenase-2 gene deletion decreasing oxidative stress injury induced by heme in vivo.Methods Stereotactic injection of 6 μ l of a sterile hemin (8 μmol/L) into the striatum of wild type and HO-2 knock out mice. Cell viability, protein oxidation, and lipid oxidation of the striatum were determined after 72 h injection. Western blot analysis was applied for heme oxygenase-1 (HO-1) measurement.Results Protein oxidation and lipid oxidation decreased significantly in HO-2 knockout mice at 72 h compared with that of wild-type mice. Striatal cell viability increased significantly in knockout mice at 72 h compared with that of wild-type mice. HO-1 expression at baseline and 72 h after hemin injection was also similar to that of wild-type mice.Conclusion These results suggest that HO-2 gene deletion protects neurons from heme mediated oxidative stress injury. Selective inhibition of neuronal HO-2 may have a beneficial effect on oxidative stress-induced neuronal injury.

关 键 词：血红素氧合酶 基因缺失 氧化应激 脑损伤 

分 类 号：R651.1[医药卫生—外科学]