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目的:研究预缺血以及联合给予预缺血和NMDA(N-甲基-D-天冬氨酸)受体抑制剂MK801后对大鼠海马CA1区Bcl-2的磷酸化以及海马CA1区锥体细胞凋亡的影响。方法:采用SD大鼠四动脉结扎全脑缺血及预缺血模型,给药组大鼠在预缺血前1h给予腹腔注射MK801 3mg/kg。用免疫印迹法分析不同处理下大鼠海马CA1区Bcl-2的蛋白表达及其磷酸化水平,焦油紫染色法分析海马CA1区锥体细胞的凋亡情况。结果:脑缺血再灌注组相对于Sham组Bcl-2的磷酸化水平以及海马CA1区锥体细胞的凋亡水平显著增高,预缺血组相对于缺血再灌注组Bcl-2的磷酸化水平以及海马CA1区锥体细胞的凋亡水平显著降低;而预缺血前给予MK801组相对于预缺血组Bcl-2磷酸化水平以及海马CA1区锥体细胞的凋亡水平显著增高;而Bcl-2的蛋白表达水平在以上不同处理条件下均无明显变化。结论:NMDA受体介导了预缺血抑制脑缺血再灌注诱导增加Bcl-2磷酸化以及海马CA1区锥体细胞凋亡。
OBJECTIVE: To investigate the effects of pre-ischemic and combined pre-ischemic and MK801 NMDA receptor antagonist on the phosphorylation of Bcl-2 in hippocampal CA1 region of rat hippocampus and the cone of hippocampal CA1 region Effect of somatic cell apoptosis. Methods: The model of global cerebral ischemia and preconditioning was induced by four rats in SD rats. The rats in the administration group were intraperitoneally injected with MK801 3mg / kg 1h before pre-ischemia. Western blotting was used to analyze the protein expression and phosphorylation of Bcl-2 in hippocampal CA1 region of rats under different treatment, and the apoptosis of pyramidal cells in hippocampal CA1 region was analyzed by using tar violet staining. Results: The phosphorylation of Bcl-2 and the apoptosis of hippocampal CA1 pyramidal neurons in cerebral ischemia-reperfusion group were significantly higher than those in Sham group. Compared with ischemia-reperfusion group, Bcl-2 phosphorylation Level and hippocampal CA1 pyramidal cell apoptosis levels were significantly reduced; while pre-ischemic preconditioning MK801 group compared with pre-ischemic Bcl-2 phosphorylation and hippocampal CA1 pyramidal cell apoptosis was significantly increased; and The protein expression level of Bcl-2 had no significant change under the above different treatment conditions. CONCLUSION: NMDA receptor mediates preconditioning inhibition of cerebral ischemia-reperfusion-induced increase of Bcl-2 phosphorylation and apoptosis of pyramidal cells in hippocampal CA1 region.