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目的:研究脑缺血再灌注以及联合给予脑缺血和NMDA(N-甲基-D-天冬氨酸)受体抑制剂MK801对大鼠海马CA1区Glu R6巯基亚硝基化以及海马CA1区锥体细胞凋亡的影响。方法:采用四动脉结扎法构建大鼠全脑缺血再灌注模型,给予SD大鼠腹腔注射NMDA受体特异性抑制剂MK801(3 mg/kg)。主要运用’生物素转化法’(Biotin-Switch method)、SDS-PAGE、免疫印迹、焦油紫染色等方法对Glu R6的巯基亚硝基化(S-亚硝基化)、蛋白表达水平以及海马CA1区锥体细胞的凋亡水平进行研究。结果:脑缺血/再灌注显著促进Glu R6的巯基亚硝基化以及海马CA1区锥体细胞的凋亡,给予NMDA受体特异性抑制剂MK801能够显著抑制脑缺血/复灌诱导增加的Glu R6的S-亚硝基化以及海马CA1区锥体细胞的凋亡。结论:脑缺血/再灌注早期NMDA受体介导了Glu R6的巯基亚硝基化以及海马CA1区锥体细胞的凋亡,从而为临床治疗缺血再灌注脑损伤提供了理论依据。
AIM: To investigate the effects of cerebral ischemia-reperfusion and combined administration of MK801, an inhibitor of NMDA (N-methyl-D-aspartate) receptor, on nitrosylation of Glu and R6 in hippocampal CA1 region of hippocampus and hippocampal CA1 Effect of Apoptosis in District Pyramidal Cells. Methods: The rat model of global cerebral ischemia-reperfusion was established by four-artery ligation. SD rats were injected intraperitoneally with NMDA receptor-specific inhibitor MK801 (3 mg / kg). The nitrosylation (S-nitrosylation) of Glu R6 and the expression of protein in hippocampus were mainly carried out by Biotin-Switch method, SDS-PAGE, Western blotting and tar violet staining CA1 pyramidal cells apoptosis levels were studied. Results: Cerebral ischemia / reperfusion could significantly promote the sulfhydryl nitrosylation of Glu R6 and the apoptosis of pyramidal cells in hippocampal CA1 region. Administration of MK801, a specific inhibitor of NMDA receptor, could significantly inhibit the increase of cerebral ischemia-reperfusion-induced S-nitrosylation of Glu R6 and apoptosis of pyramidal cells in hippocampal CA1 region. CONCLUSION: NMDA receptor mediates the thiol nitrosylation of Glu R6 and the apoptosis of pyramidal cells in hippocampal CA1 area in the early stage of cerebral ischemia / reperfusion, which provides a theoretical basis for the clinical treatment of cerebral ischemia-reperfusion injury.