Protective effects of alpinae Oxyphyllae Fructus (Alpinia oxyphylla MIQ) water-extracts on neurons from ischemic damage and neuronal cell toxicity

被引:65
作者
Koo, BS
Lee, WC
Chang, YC
Kim, CH
机构
[1] Dongguk Univ COM, NRL Glycobiol, Dept Biochem Mol Biol & Neurobiol, Kyungju 780714, Kyungbuk, South Korea
[2] Minist Sci & Technol Korea, Natl Res Lab Glycobiol, Kyungju, Kyungbuk, South Korea
[3] Keimyung Univ, Coll Med, Kidney Inst, Jung Gu, Taegu, South Korea
关键词
alpinae Oxyphyllae Fructus; Alpinia oxyphylla MIQ; cerebrovascular disorder; primary neuron; lipid peroxidation; A beta; N-methyl-D-aspartate receptor; glutamate toxicity; ischemia; hippocampal CA1; intracellular Ca2+; NO;
D O I
10.1002/ptr.1382
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Alpinae Oxyphyllae Fructus (Alpinia oxyphylla MIQ) (Korean name Ik-Jj-In) is a medicinal plant used in Korea for the treatment of various symptoms accompanying hypertension and cerebrovascular disorders. The present study was performed to investigate the effects of Alpinae Oxyphyllae Fructus water-extracts (AOF) on a cultured primary neuron cell system, cell cytotoxicity and lipid peroxidation in Abeta treatment conditions. Cell killing was significantly enhanced by addition of increasing concentrations of Abeta. Pretreatment of AOF attenuated in cell killing enhanced by increasing concentrations of Abeta. Abeta-induced cell death was protected by the application of water extract of AOF in a dose-dependent manner, and concentrations of 50 to 100 mug/ml had a significant effect compared to exposure of Abeta only. AOF has been shown to protect primary cultured neurons from N-methyl-D-aspartate (NMDA) receptor-mediated glutamate toxicity. The evidence indicated that AOF protects neurons against ischemia-induced cell death. Oral administration of AOF into mice prevented ischemia-induced learning disability and rescued hippocampal CA1 neurons from lethal ischemic damage. The neuroprotective action of exogenous AOF was also confirmed by counting synapses in the hippocampal CA1 region. The presence of AOF in neuron cultures did not repress a NMDA receptor-mediated increase in intracellular Ca2+, but rescued the neurons from NO-induced death. AOF may exert its neuroprotective effect by reducing the NO-mediated formation of free radicals or antagonizing their toxicity. Copyright (C) 2004 John Wiley Sons, Ltd.
引用
收藏
页码:142 / 148
页数:7
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