Heme oxygenase-2 gene deletion protects basal ganglia cells from oxidative injury induced by free Fe2+
10.3321/j.issn:0258-879X.2005.04.010
- VernacularTitle:血红素加氧酶-2基因敲除对Fe2+诱导的小鼠脑氧化应激损伤中基底节细胞的保护作用
- Author:
Yan QU
1
;
Xiang ZHANG
;
Jian-Ning ZHANG
;
Hai-Ning ZHEN
;
Da-Kuan GAO
Author Information
1. 第四军医大学附属西京医院
- Keywords:
heme oxygenase;
brain edema;
oxidative injury;
gene knockout
- From:
Academic Journal of Second Military Medical University
2005;26(4):390-395
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To determine whether heme oxygenase-2(HO-2) gene deletion can attenuate oxidative injury induced by free Fe2+. Methods:Stereotactic injection of 10 μl sterile FeCl2 (10 mmol/L) was made into the right striata of HO-2 knockout mice and wild-type mice. Brain edema severity was measured at 24 h. Cell viability, protein oxidation, and lipid oxidation of the basal ganglia were determined at 72 h. Western blot analysis was applied for heme oxygenase-1 (HO-1) measurement.Results: Brain water content significantly decreased in HO-2 knockout mice at 24 h compared with wild-type mice. Protein oxidation and lipid oxidation significantly decreased in HO-2 knockout mice at 72 h compared with wild-type mice, while the striatal cell viability increased significantly. HO-1 expression at baseline and 72 h was also similar to that in wild-type mice. Conclusion:These results show that HO-2 gene deletion can protect basal ganalia cells from free Fe2+ -mediated oxidative stress injury,suggesting that selective inhibition of HO-2 may have a protective effect on brain oxidative injury.
