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Cited 34 time in webofscience Cited 35 time in scopus
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Protection Against Kainate Neurotoxicity by Ginsenosides: Attenuation of Convulsive Behavior, Mitochondrial Dysfunction, and Oxidative Stress

Authors
Shin, Eun-JooJeong, Ji HoonKim, A-YoungKoh, Young HoNah, Seung-YeoulKim, Won-KiKo, Kwang HoKim, Hyun JiWie, Myung-BokKwon, Yong SooYoneda, YukioKim, Hyoung-Chun
Issue Date
15-Feb-2009
Publisher
WILEY-BLACKWELL
Keywords
GSH/GSSG; ultrastructural degeneration; hippocampus; Mn-superoxide dismutase; mitochondrial membrane potential
Citation
JOURNAL OF NEUROSCIENCE RESEARCH, v.87, no.3, pp 710 - 722
Pages
13
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF NEUROSCIENCE RESEARCH
Volume
87
Number
3
Start Page
710
End Page
722
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/16229
DOI
10.1002/jnr.21880
ISSN
0360-4012
1097-4547
Abstract
We previously demonstrated that kainic acid (KA)-mediated mitochondrial oxidative stress contributed to hippocampal degeneration and that ginsenosides attenuated KA-induced neurotoxicity and neuronal degeneration. Here, we examined whether ginsenosides affected KA-induced mitochondrial dysfunction and oxidative stress in the rat hippocampus. Treatment with ginsenosides attenuated KA-induced convulsive behavior dose-dependently. KA treatment increased lipid peroxidation and protein oxidation and decreased the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio to a greater degree in the mitochondrial fraction than in the hippocampal homogenate. KA treatment resulted in decreased Mn-superoxide dismutase expression and diminished the mitochondrial membrane potential. Furthermore, KA treatment increased intramitochondrial Ca2+ and promoted ultrastructural degeneration in hippocampal mitochondria. Treatment with ginsenosides dose-dependently attenuated convulsive behavior and the KA-induced mitochondrial effects. Protection appeared to be more evident in mitochondria than in tissue homogenates. Collectively, the results suggest that ginsenosides prevent KA-induced neurotoxicity by attenuating mitochondrial oxidative stress and mitochondrial dysfunction. (C) 2008 Wiley-Liss,inc.
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