Protection Against Kainate Neurotoxicity by Ginsenosides: Attenuation of Convulsive Behavior, Mitochondrial Dysfunction, and Oxidative Stress
DC Field | Value | Language |
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dc.contributor.author | Shin, Eun-Joo | - |
dc.contributor.author | Jeong, Ji Hoon | - |
dc.contributor.author | Kim, A-Young | - |
dc.contributor.author | Koh, Young Ho | - |
dc.contributor.author | Nah, Seung-Yeoul | - |
dc.contributor.author | Kim, Won-Ki | - |
dc.contributor.author | Ko, Kwang Ho | - |
dc.contributor.author | Kim, Hyun Ji | - |
dc.contributor.author | Wie, Myung-Bok | - |
dc.contributor.author | Kwon, Yong Soo | - |
dc.contributor.author | Yoneda, Yukio | - |
dc.contributor.author | Kim, Hyoung-Chun | - |
dc.date.available | 2019-05-30T03:37:59Z | - |
dc.date.issued | 2009-02 | - |
dc.identifier.issn | 0360-4012 | - |
dc.identifier.issn | 1097-4547 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/23316 | - |
dc.description.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. | - |
dc.format.extent | 13 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | WILEY-BLACKWELL | - |
dc.title | Protection Against Kainate Neurotoxicity by Ginsenosides: Attenuation of Convulsive Behavior, Mitochondrial Dysfunction, and Oxidative Stress | - |
dc.type | Article | - |
dc.identifier.doi | 10.1002/jnr.21880 | - |
dc.identifier.bibliographicCitation | JOURNAL OF NEUROSCIENCE RESEARCH, v.87, no.3, pp 710 - 722 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000263190100014 | - |
dc.identifier.scopusid | 2-s2.0-62849096825 | - |
dc.citation.endPage | 722 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 710 | - |
dc.citation.title | JOURNAL OF NEUROSCIENCE RESEARCH | - |
dc.citation.volume | 87 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | GSH/GSSG | - |
dc.subject.keywordAuthor | ultrastructural degeneration | - |
dc.subject.keywordAuthor | hippocampus | - |
dc.subject.keywordAuthor | Mn-superoxide dismutase | - |
dc.subject.keywordAuthor | mitochondrial membrane potential | - |
dc.subject.keywordPlus | SENESCENCE-ACCELERATED MICE | - |
dc.subject.keywordPlus | RAT HIPPOCAMPUS | - |
dc.subject.keywordPlus | GLUTATHIONE HOMEOSTASIS | - |
dc.subject.keywordPlus | NEURONAL DEGENERATION | - |
dc.subject.keywordPlus | CA2+ CHANNELS | - |
dc.subject.keywordPlus | GRANULE CELLS | - |
dc.subject.keywordPlus | GINSENG ROOT | - |
dc.subject.keywordPlus | BRAIN-INJURY | - |
dc.subject.keywordPlus | CALCIUM | - |
dc.subject.keywordPlus | SEIZURES | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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