摘要
目的:观察血红素加氧酶2基因敲除对脑出血后损伤的保护作用。方法:应用血红素加氧酶2基因敲除小鼠,制备脑出血模型。利用MTT法测量出血区域细胞生存率,利用蛋白印记法检测出血区域脑组织氧化反应性蛋白及脂质氧化蛋白含量。结果:血红素加氧酶2基因敲除小鼠出血区域细胞生存率显著高于野生型小鼠,血红素加氧酶2基因敲除小鼠出血区域组织氧化反应性蛋白及脂质氧化蛋白含量显著低于野生型小鼠。结论:血红素加氧酶2参与了脑出血后氧化应激损伤,敲除血红素加氧酶2基因对脑出血损伤具有保护作用。
Objective：To investigate neuroprotective effect of heine oxygenase-2（HO-2） gene knockout on in tracerebral hemorrhage inmouse. Methods： An intracerebral hemorrhagic model was established in the HO-2 knock out mouse. Cell viability, protein oxidation and lipid oxidation of the injury area were determined. Results： protein oxidation and lipid oxidation decreased significantly in HO-2 knockout mice compared with wild-type mice after injury, but cell viability increased significantly in the knockout mice after injury compared with wild-type mice. Conclusions： These results suggest that HO-2 gene deletion protects brain cells from hemorrhagic injury.Selective inhibition of neuronal HO-2 may have a beneficial effect on intracerebral hemorrhagic injury.
出处
《西南国防医药》
CAS
2005年第2期117-122,共6页
Medical Journal of National Defending Forces in Southwest China
关键词
血红素加氧酶
脑出血
氧化应激损伤
基因敲除
heine oxygenase, intracerebral hemorrhage, oxidative injury, gene knockout
