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摘要Objective To make an ischemical reperfusion injury model in cultured rat hippocampal neurons and observe the expression of NMDA receptor subunits NR1, NR2B and glutamate of rat hippocampal neurons after ischemical reperfusion injury 24h,48h and 72h. To study the pathogenesy of ischemical reperfusion injury and the effects of ginsenoside Rg2 on injured neurons on the aspect of excitotoxicity of excitatory amino acid especially the expression of receptor subunits. Methods To make an ischemical reperfusion injury model by oxygen and glucose deprivation (OGD) in cultured rat hippocampal neurons. Nissl's staining was used to identify hippocampal neurons. The injury of neurons was detected by the MTT reduction assay method after OGD. The expression of receptor subunits NR1, NR2B and glutamate was detected by immunocytochemical technique. Laser scanning confocal microscope and Fluo-3/AM were used to measure the intracellular calcium fluorescence pixel values of hippocampal neurons. Results The activity of neurons was decreased in model group than in control group (P＜0.05). The longer was the reperfusion time the lower was the activity of neurons. The release of glutamate from damaged neurons was increased significantly comparing with control group(P＜0.05). The expression of receptor subunits NR1 was increased and that of receptor subunits NR2B was decreased comparing with the control group(P＜0.05). The fluorescence pixel value of intracellular free calcium of hippocampal neurons was significantly higher after OGD(P＜0.05). The activity of neurons was increased significantly in hippocampal neurons treated by ginsenoside Rg2(P＜0.05). The release of glutamate from neurons treated by ginsenoside Rg2 was decreased significantly comparing with the model group (P＜0.05). The [Ca2+]i and the expression of NR1 decreased and the expression of NR2B increased comparing with the model group (P＜0.05) Conclusions The release of glutamate increased which activated the excitatory amino acid receptors excessively in ischemical reperfusion injured hippocampal neurons. The expression of receptor subunits NR1 was increased and that of receptor subunits NR2B was decreased, which induced the function change of the receptors and resulted in the [Ca2+]i overloading after the injury. All this induced the injury of the neurons caused by a series of biochemical event depending Ca2+ intra-cellular. Ginsenoside Rg2 plays its protective role in inhibiting the release of glutamate, regulating the expression of excitatory amino acid receptors subunits, reducing the influx of calcium ion, and increasing the activity of neurons.