低氧预适应保护缺血脑组织效应中CaMKⅡ的作用.pdfVIP

二校 136 Tianjin Med J,Feb 2013,Vol 41 No 2 doi:10.3969/j.issn.0253-9896.2013.02.000 * 低氧预适应保护缺血脑组织效应中CaMK Ⅱ的作用机制 1 2 2 2 2 △ 李海涛 卜祥宁 江 君 杨巍巍 李俊发 【摘要】 目的 探讨钙调蛋白依赖性蛋白激酶Ⅱ( CaMK Ⅱ)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，应用Western blot 并结合Gel Doc 凝胶成像系统定量检测4 组小鼠脑组织内CaMK Ⅱ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CaMK Ⅱ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CaMK Ⅱ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CaMK Ⅱ磷酸化 水平及p-CaMK Ⅱ阳性细胞数目高于常氧缺血组(P 0.05) 。结论 HPC 减缓缺血半影区CaMK Ⅱ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。 脑低氧预适应；脑中动脉梗塞；CaMK Ⅱ；磷酸化水平；蛋白表达量 【关键词】 Mechanisms of CaMK Ⅱin the Hypoxic Preconditioning Protection of Ischemic Brain Tissue LI Haitao BU Xiangning JIANG Jun YANG Weiwei LI Junfa DepartmentofPhysiology,YanjingMedicalCollege,CapitalMedicalUniversity,Beijing101300,China [Abstract] 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 (H0-sham) group, HPC-sham group, H0-ischemia group and HPC-ischemia group. Changes of CaMK Ⅱphosphoryla⁃ tion in the brain of mice were detected by Western blot combined with Gel Doc imagine systems. Levels of CaMK Ⅱphos⁃ phorylation in brain cortex of mice were detected by immunohistochemistry. Results Both phosphorylation and protein ex⁃ pression l