[Glutamate-related mechanism of ginsenosides against anoxic-ischemic brain damage].
[Glutamate-related mechanism of ginsenosides against anoxic-ischemic brain damage].
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发表时间：
2001-05
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通讯作者：
Z. L. Jiang;Y. Chen;C. Zhou;J. S. Shi;S. Duan
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作者：
Z. L. Jiang;Y. Chen;C. Zhou;J. S. Shi;S. Duan
目的与方法观察黄芪总苷对谷氨酸兴奋性神经毒性的拮抗作用，以及在模拟缺血条件下，黄芪总苷对培养的小鼠皮层神经元谷氨酸释放和星形胶质细胞谷氨酸摄取的抑制和促进作用。目的：探讨黄芪总皂苷对缺氧缺血性脑损伤的保护作用是否与降低谷氨酸的兴奋性神经毒性有关。结果谷氨酸（1 mmol/L）作用20 min后，海马脑片记录到的顺向群体棘波（OPS）振幅降低并最终消失，1h后恢复。然而，在使用不同浓度的黄芪皂苷后，OPS恢复良好，特别是在20 μ g/ml。在培养的小鼠皮层神经元和星形胶质细胞中，模拟缺血时神经元释放的谷氨酸是对照组的数倍，星形胶质细胞摄取的谷氨酸明显减少，黄芪皂甙（20 μ g/ml）可显著抑制神经元释放的谷氨酸，促进星形胶质细胞摄取谷氨酸。结论减轻谷氨酸的兴奋性神经毒性可能是黄芪皂甙抗缺氧缺血性脑损伤的重要机制。
AIM AND METHODS To observe the antagonist effect of ginsenosides upon excitatory neurotoxicity of glutamate in rat hippocampal slices, and to observe the inhibitory and facilitated effects of ginsenosides upon glutamate release from cultured mice cortical neurons and upon glutamate uptake by cultured astrocytes, respectively, during simulated ischemia, in order to elucidate whether the protective effect of ginsenosides against anoxic-ischemic brain damage is related to reducing the excitatory neurotoxicity of glutamate. RESULTS The orthodromic population spikes (OPS) recorded in hippocampal slice decreased in amplitude and disappeared finally during 20-min glutamate (1 mmol/L) exposure, and recovered less 1 h after the end of this exposure. However, OPS recovered well after the use of ginsenosides at different concentrations, especially at 20 microg/ml. In cultured mice cortical neurons and astrocytes, glutamate released from neurons up to several times of control and its uptake by astrocytes decreased markedly during simulated ischemia, ginsenosides (20 microg/ml) could significantly inhibit glutamate release from neurons and facilitate glutamate uptake by astrocytes during the same ischemia exposure. CONCLUSIONS Reducing the excitatory neurotoxicity of glutamate may be an important mechanism of ginsenosides against anoxic-ischemic brain damage.