Protection Against Kainate Neurotoxicity by Ginsenosides: Attenuation of Convulsive Behavior, Mitochondrial Dysfunction, and Oxidative Stress
- Authors
- Shin, Eun-Joo; Jeong, Ji Hoon; Kim, A-Young; Koh, Young Ho; Nah, Seung-Yeoul; Kim, Won-Ki; Ko, Kwang Ho; Kim, Hyun Ji; Wie, Myung-Bok; Kwon, Yong Soo; Yoneda, Yukio; Kim, Hyoung-Chun
- Issue Date
- 15-2월-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
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF NEUROSCIENCE RESEARCH
- Volume
- 87
- Number
- 3
- Start Page
- 710
- End Page
- 722
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/120576
- DOI
- 10.1002/jnr.21880
- ISSN
- 0360-4012
- 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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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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