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目的:观察血红素加氧酶2 基因敲除对Fe2+诱导的脑氧化应激损伤的保护作用。方法:采用立体定向法注射10μl FeCl2(10 mmol/L)至血红素加氧酶2 基因敲除小鼠及野生型小鼠右侧纹状体,制备Fe2+诱导的脑氧化应激损伤模型。测量损伤24 h后损伤区域脑水肿程度。利用MTT法测量损伤72 h后细胞生存率。利用蛋白印迹法检测损伤72 h后细胞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 基因敲除小鼠脑水肿程度显著低于野生型小鼠;损伤区域细胞生存率显著高于野生型小鼠;血红素加氧酶2 基因敲除小鼠损伤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Fe2+诱导的脑氧化应激损伤,基因敲除血红素加氧酶2 对脑氧化应激损伤具有保护作用。
Objective: To observe the protective effect of heme oxygenase 2 gene knockout on Fe2 + -induced cerebral oxidative stress injury. Methods: Fe2 + -induced cerebral oxidative stress injury model was prepared by injecting 10μl FeCl2 (10 mmol / L) into heme oxygenase 2 gene knockout mice and wild type mice right striatum by stereotactic method. The extent of brain edema in the damaged area was measured 24 h after injury. Cell viability was measured by MTT assay 72 h after injury. Western blotting was used to detect the contents of oxidized protein and lipid oxidized protein in brain tissue after 72 h of injury. Results: The degree of brain edema in heme oxygenase-2 knockout mice was significantly lower than that in wild type mice. The cell survival rate in injured area was significantly higher than that in wild type mice. The heme oxygenase 2 knockout mice injury area Tissue oxidative protein and lipid oxidation protein content was significantly lower than wild-type mice. Conclusion: Heme oxygenase 2 is involved in Fe2 + -induced cerebral oxidative stress injury. Gene knockdown heme oxygenase 2 has a protective effect on cerebral oxidative stress injury.