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目的探讨神经节苷脂（ＧＭ１）的脑保护作用及其可能机制。方法用四血管闭塞（４ＶＯ）全脑缺血再灌注模型，用高效液相色谱仪柱前衍生色谱法测定假手术组、缺血３０ｍｉｎ再灌注６０ｍｉｎ生理盐水（ＮＳ）处理组、缺血３０ｍｉｎ再灌注６０ｍｉｎＧＭ１处理组的海马组织兴奋性氨基酸（ＥＡＡ）含量，并观察缺血３０ｍｉｎ再灌注４ｄ海马ＣＡ１区病理变化。结果缺血再灌注ＮＳ处理组海马组织ＥＡＡ含量显著性降低（Ｐ＜０．０１），海马ＣＡ１区多数神经元坏死，残存神经元呈较严重缺血性改变，ＧＭ１处理组上述生化病理改变明显为轻。结论推测ＧＭ１可调控缺血再灌注早期ＥＡＡ的过度释放和（或）重摄取受阻，减轻其在细胞外堆聚引起的兴奋毒性损伤，具有脑保护作用。
Objective To explore the neuroprotective effect of ganglioside (GM1) and its possible mechanism. Methods Four - vessel occlusion (4VO) model of global cerebral ischemia - reperfusion was established. The rats in sham - operated group were pretreated with high performance liquid chromatography (HPLC) The content of excitatory amino acid (EAA) in the hippocampus of 60minGM1-treated group was perfused, and the pathological changes of hippocampal CA1 area were observed at 30min after reperfusion. Results The levels of EAA in hippocampus of NS group were significantly decreased (P <0.01), most of the neurons in hippocampal CA1 area were necrotic, the residual neurons showed more severe ischemic changes, and the above biochemical and pathological changes were obvious in GM1-treated group Light. CONCLUSIONS: GM1 can regulate the over-release and / or reuptake of EAA during the early stage of ischemia-reperfusion, and reduce the excitotoxicity induced by GM-induced accumulation of GM1.