脑缺血预处理对大鼠海马CA1区肌细胞促进因子2C磷酸化水平的影响

EFFECT OF CEREBRAL ISCHEMIA PRECONDITIONING ON MYOCYTE ENHANCER FACTOR 2C ACTIVATION IN RAT HIPPACOMPAL CA1 REGION

目的现察大鼠全脑缺血预处理后不同时间点海马CA1区肌细胞促进因子(Myocyte enhancer factor,MEF)2C磷酸化(激活)的变化规律。方法建立Sprague-Dawley大鼠四动脉结扎全脑缺血模型,大鼠随机分成二组,对照组(sham组)和实验组(脑缺血预处理组)。采用免疫印迹法和免疫组织化学方法检测实验组MEF2C磷酸化水平。结果全脑缺血预处理(3min)48h后再次严重缺血6min,复灌6h、1d、3d、5d海马CA1区MEF2C激活均高于对照组,3d达到最高峰。免疫组织化学结果显示,预处理后的1d磷酸化的MEF2C主要分布在细胞核。结论海马CA1区MEF2C磷酸化水平的升高可能参与了脑缺血耐受保护机制的形成。

Objective To investigate the phosphorylation of myocyte enhancer factor（MEF） 2C in hippocampus CA1 region of rat brain at different time points after ischemic preconditioning. Methods SD rats were divided into two groups randomly, sham group and ischemic preconditioning group. The phosphorylation levels of MEF 2C in hippocampal CA1 region were detected by Western blotting or Immunohistochemistry. Results After the treatment of 6h, 1, 3, and 5d in the experimental groups, MEF2C phosphorylation levels increased to its peak at 3d compared with sham group. At ld of reperfusion after CIP（C, D） ,p- MEF2C immunoreactlgity increased markedly in the nucleus compared with that of the sham group. Conclu- sion Accumulating evidence documents that MEF2C protein is activated by MAP kinases and has been proposed to play a critical role in neuronal survival. In conclusion, our current results indicated that the increasing activation of MEF2C might be one of the important factors inducing cerebral ischemic tolerance mechanism.