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目的：观察单唾液酸四已糖神经节苷胸（GM1）对脑缺血再灌注损伤的保护作用。方法：采用四血管闭塞（4VO）全脑缺血再灌注动物模型，测定假手术组，缺血30min再灌注60minGM1；处理组（10mg／kg，缺血5min腹腔注射），缺血30min再灌注60min生理盐水（NS）处理组鼠脑海马组织兴奋性氨基酸（ExcitatoryAminoAcid，EAA），钙调素（Calmodulin，CaM），丙二醛（Malondiadehyde，MDA）的含量。结果：脑缺血再灌注组海马组织EAA含量显著性降低（P〈0．01），而CaM、MDA则显著性升高（P＜0．01），GM1处理组海马EAA、CaM、MDA含量同假术术组比较没有显著性差异（P＞0．05）。结论：GM1能阻抑脑缺血再灌注损伤中EAA的过度释放和／或重摄取障碍，细胞内外钙平衡紊乱，氧自由基产生过多等病理生理过程，发挥脑保护作用。
Objective: To observe the protective effect of monosialoglucose ganglioside (GM1) on cerebral ischemia-reperfusion injury. Methods: Four-vessel occlusion (4VO) model of global cerebral ischemia-reperfusion was established in sham-operation group. The ischemia-reperfusion 60min GMM was induced by ischemia reperfusion 30min after ischemia in the treatment group (10mg / kg, ischemia 5min) Excitatory Amino Acids (EAA), Calmodulin (CaM) and Malondiadehyde (MDA) contents in hippocampus of NS rats were measured. Results: The content of EAA in hippocampus of cerebral ischemia-reperfusion group was significantly decreased (P <0.01), while the levels of CaM and MDA were significantly increased (P <0.01). The levels of EAA, CaM and MDA Compared with the sham operation group, there was no significant difference (P> 0.05). CONCLUSION: GM1 can inhibit the over-release and / or reuptake of EAA, the imbalance of intracellular and extracellular calcium balance, and the excessive production of oxygen free radicals and other pathophysiological processes during cerebral ischemia-reperfusion injury and exert the neuroprotective effects.