Abstract
Treatment with ginsenosides attenuated KA-induced seizures and oxidative stress in the synaptosome, and reduced synaptic vesicles at the presynaptic terminals dose-dependently. The adenosine A(2A) receptor antagonist 1,3,7-trimethyl-8-(3-chlorostyryl) xanthine reversed the ginsenoside-mediated pharmacological actions. Neither the adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine nor the adenosine A(2B) receptor antagonist alloxazine affected the ginsenoside-mediated pharmacological actions. Our results suggest that ginsenosides block KA-induced synaptosomal oxidative stress, associated with hippocampal degeneration, through activation of adenosine A(2A) receptors.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine A2 Receptor Antagonists*
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Analysis of Variance
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Animals
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Caffeine / analogs & derivatives
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Caffeine / pharmacology
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Dose-Response Relationship, Drug
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Drug Interactions
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Excitatory Amino Acid Agonists
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Ginsenosides / pharmacology*
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Hippocampus / drug effects*
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Kainic Acid
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Male
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Nerve Degeneration / chemically induced
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Neuroprotective Agents / pharmacology*
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Oxidative Stress / drug effects*
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Presynaptic Terminals / drug effects
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Rats
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Rats, Sprague-Dawley
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Seizures / chemically induced
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Statistics, Nonparametric
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Synaptosomes / drug effects*
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Synaptosomes / metabolism
Substances
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Adenosine A2 Receptor Antagonists
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Excitatory Amino Acid Agonists
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Ginsenosides
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Neuroprotective Agents
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8-(3-chlorostyryl)caffeine
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Caffeine
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Kainic Acid