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低氧预适应保护缺血脑组织效应中CaMKⅡ的作用机制

李海涛   

  1. 首都医科大学燕京医学院病理生理教研室
  • 收稿日期:2012-06-26 修回日期:2012-10-16 出版日期:2013-02-15 发布日期:2013-02-15
  • 通讯作者: 李海涛

Increased Phosphorylation of CaMKⅡ in Penumbra Cerebral Tissues of HPC-MCAO Mice

LI Hai-Tao   

  1. Department of Physiology, Yanjing Medical College, Capital Medical University, Beijing 101300, China
  • Received:2012-06-26 Revised:2012-10-16 Published:2013-02-15 Online:2013-02-15
  • Contact: LI Hai-Tao

摘要:

【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 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(P < 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。

关键词: 脑低氧预适应, 脑中动脉梗塞, CaMKⅡ, 磷酸化水平, 蛋白表达量

Abstract:

[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 kinaseⅡ(CaMKⅡ) phosphorylation thereof. Methods  Thirty-six healthy male BALB/c mice were randomly divided into 4 groups: the normoxic sham surgery (H0-sham) group, HPC-sham group, H0-ischemia group and HPC-ischemia group. Changes of CaMKⅡ phosphorylation in the brain of mice were detected by Western blot combined with Gel Doc imagine systems. Levels of CaMK Ⅱ phosphorylation in brain cortex of mice were detected by immunohistochemistry. Results  Both phosphorylation and protein expression levels in the ischemic core and penumbra were significantly decreased in H0-ischemia group compared with those in H0-sham group (P < 0.05). But the phosphorylation levels of CaMKⅡ and the positive cell number of p - CaMK Ⅱin the penumbra were significantly higher in HPC-ischemia group than those of H0-ischemia group (P < 0.05). Conclusion  The de? creased CaMKⅡ phosphorylation level in ischemia penumbra might involve in the attenuation of middle cerebral artery occlusion (MCAO)-induced brain injury in mice.

Key words: Cerebral hypoxic preconditioning, MCAO, CaMKⅡ, Phosphorylation, Protein expression