鼠脑缺血时氧化还原因子-1蛋白的表达

The expression of Ref-1 protein in experimental cerebral ischemia

目的 观察大鼠永久性脑缺血后不同时相脑组织氧化还原因子 1蛋白的表达特性。方法 采用线栓法制作大鼠大脑中动脉阻断模型 ,以尾壳核平面为模板 ,采用免疫组化方法 ,观察正常对照组、假手术组及缺血 1、6、12、2 4和 4 8h氧化还原因子 1蛋白阳性染色细胞的分布部位及数量。结果 免疫组织化学染色显示 ,正常对照组、假手术组、左侧大脑半球氧化还原因子 1蛋白在细胞核表达 ;而缺血组 ,在梗死中心的坏死区无氧化还原因子 1蛋白表达 ;在半暗带区 ,氧化还原因子 1蛋白表达随缺血时间的延长而下降 ,各时间点间差异有显著意义。结论 脑缺血后 ,半暗带区氧化还原因子 1蛋白免疫活性下降和DNA修复机制的失败 ,考虑与局灶性脑缺血半暗带区细胞凋亡的发生有关。

Objective To explore the characteristic of the expression of Ref 1 protein in different intervals following permanent focal cerebral ischemia in rats. Methods The model of the middle cerebral artery occlusion (MCAO) in rats was performed with the intraluminal filament occlusion The rat brains were cut in the coronal planes at the levels of the caudate putamen as the templates The immunohistochemistry staining was used to facilitate the observation of the distribution and quantities of Ref 1 protein expression in the brain tissues following the normal control group,sham operation group and the permanent MCAO group with intervals of 1, 6, 12, 24 h, and 48 h, respectively. Results Immunohistochemistry showed the nuclear expression of Ref 1 protein in the normal control group, sham operation group and left cerebral hemisphere. In the ischemic group, there was no immunoreactivity of Ref 1 protein in the core of infarction, and nuclear immunoreactivity of Ref 1 protein was decreased along with the extension of ischemic time in the penumbra. The difference among those groups was significant ( P <0.05). Conclusion Our results suggest that the rapid decrease of Ref 1 and the failure of DNA repairing mechanism may be contributed to the apoptosis in penumbra after focal cerebral ischemia