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Protective effects of alpinae oxyphyllae fructus ( Alpinia oxyphylla MIQ) water‐extracts on neurons from ischemic damage and neuronal cell toxicity
Author(s) -
Koo ByungSoo,
Lee WonChang,
Chang YoungChae,
Kim CheorlHo
Publication year - 2004
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.1382
Subject(s) - neuroprotection , pharmacology , neuron , nmda receptor , toxicity , programmed cell death , glutamate receptor , hippocampal formation , cytotoxicity , neurotoxicity , cell damage , lipid peroxidation , receptor , pharmacognosy , biology , chemistry , medicine , apoptosis , antioxidant , biochemistry , neuroscience , biological activity , in vitro
Abstract 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 A β treatment conditions. Cell killing was signicantly enhanced by addition of increasing concentrations of A β . Pretreatment of AOF attenuated in cell killing enhanced by increasing concentrations of A β . A β ‐induced cell death was protected by the application of water extract of AOF in a dose‐dependent manner, and concentrations of 50 to 100 µg/ml had a signicant effect compared to exposure of A β 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 conrmed 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 Ca 2+ , 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 © 2004 John Wiley & Sons, Ltd.