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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-JooKoh, Young HoKim, A-YoungNah, Seung-YeoulJeong, Ji HoonChae, Jong-SeokKim, Sun CheolYen, Tran Phi HoangYoon, Hyoung-JongKim, Won-KiKo, Kwang-HoKim, 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
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/120726
DOI
10.1016/j.bbr.2008.08.038
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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