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Ginsenosides attenuate kainic acid-induced synaptosomal oxidative stress via stimulation of adenosine A(2A) receptors in rat hippocampus
- Authors
- Shin, Eun-Joo; Koh, Young Ho; Kim, A-Young; Nah, Seung-Yeoul; Jeong, Ji Hoon; Chae, Jong-Seok; Kim, Sun Cheol; Yen, Tran Phi Hoang; Yoon, Hyoung-Jong; Kim, Won-Ki; Ko, Kwang-Ho; Kim, Hyoung-Chun
- Issue Date
- 30-1월-2009
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- Ginsenosides; Kainate; Synaptosome; Oxidative stress; Hippocampus; Adenosine A(2A) receptor
- Citation
- BEHAVIOURAL BRAIN RESEARCH, v.197, no.1, pp.239 - 245
- Indexed
- SCIE
SCOPUS
- Journal Title
- BEHAVIOURAL BRAIN RESEARCH
- Volume
- 197
- Number
- 1
- Start Page
- 239
- End Page
- 245
- ISSN
- 0166-4328
- 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. (c) 2008 Elsevier B.V. All rights reserved.
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