中文摘要：

目的探讨钙调蛋白依赖性蛋白激酶Ⅱ（CaMKⅡ）在低氧预适应（HPC）保护小鼠缺血脑组织中的作用。方法36只健康雄性BALB／c小鼠随机分为常氧假手术组、HPC假手术组、常氧缺血组和HPC缺血组，每组6只应用Westemblot并结合GelDoc凝胶成像系统定量检测4组小鼠脑组织内CaMKⅡ蛋白表达量和磷酸化水平的变化，用免疫组化检测常氧缺血组和HPC缺血组小鼠脑皮层CaMKⅡ磷酸化水平。结果与常氧假手术组相比，常氧缺血组小鼠皮层缺血核心区和半影区CaMKⅡ蛋白表达量和磷酸化水平均显著降低（P〈0．05），HPC缺血组缺血半影区CaMKⅡ磷酸化水平及p-CaMKⅡ阳性细胞数目高于常氧缺血组（尸〈0．05）。结论HPC减缓缺血半影区CaMKⅡ磷酸化水平的降低，可能参与减轻因中脑动脉闭塞所致小鼠缺血性脑损伤作用。

英文摘要：

Objective To investigate the effect of hypoxic preconditioning （HPC） on middle cerebral artery occlusion （MCAO）-induced brain injury in mice, and changes of calcium/calmodulin-dependent protein kinase II （CaMK Ⅱ ） phosphory- lation thereof. Methods Thirty-six healthy male BALB/c mice were randomly divided into 4 groups： the normoxic sham sur- gery （HO-sham） group, HPC-sham group, HO-ischemia group and HPC-ischemia group. Changes of CaMK Ⅱ phosphoryla- tion in the brain of mice were detected by Western blot combined with Gel Doc imagine systems. Levels of CaMK Ⅱ phos- phorylation in brain cortex of mice were detected by immunohistochemistry. Results Both phosphorylation and protein ex- pression levels in the ischemic core and penumbra were significantly decreased in HO-ischemia group compared with those in HO-sham group （P〈 0.05）. But the phosphorylation levels of CaMK Ⅱ and the positive cell number ofp - CaMK Ⅱ in the pen- umbra were significantly higher in HPC-ischemia group than those of HO-ischemia group （P 〈 0.05）. Conclusion The de- creased CaMK Ⅱ phosphorylation level in ischemia penumbra might involve in the attenuation of middle cerebral artery occlu- sion （MCAO）-induced brain injury in mice.