Ginsenosides attenuate kainic acid-induced synaptosomal oxidative stress via stimulation of adenosine A2A receptors in rat hippocampus

Eun Joo Shin, Young Ho Koh, A. Young Kim, Seung Yeoul Nah, Ji Hoon Jeong, Jong Seok Chae, Sun Cheol Kim, Tran Phi Hoang Yen, Hyoung Jong Yoon, Won Ki Kim, Kwang Ho Ko, Hyoung Chun Kim

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)

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 A2A receptor antagonist 1,3,7-trimethyl-8-(3-chlorostyryl) xanthine reversed the ginsenoside-mediated pharmacological actions. Neither the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine nor the adenosine A2B 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 A2A receptors.

Original languageEnglish
Pages (from-to)239-245
Number of pages7
JournalBehavioural Brain Research
Volume197
Issue number1
DOIs
Publication statusPublished - 2009 Jan 30

Bibliographical note

Funding Information:
This study was supported by a grant (M103KV010013-08K2201-01310) from the Brain Research Center from 21st Century Frontier Research Program funded by the Ministry of Science and Technology, Republic of Korea. JS Chae and SC Kim were supported by BK 21 program. Equipment at the Institute of Pharmaceutical Science in the Kangwon National University was used for this study.

Copyright:
Copyright 2009 Elsevier B.V., All rights reserved.

Keywords

  • Adenosine A receptor
  • Ginsenosides
  • Hippocampus
  • Kainate
  • Oxidative stress
  • Synaptosome

ASJC Scopus subject areas

  • Behavioral Neuroscience

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