Chrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chae, Unbin | - |
dc.contributor.author | Min, Ju-Sik | - |
dc.contributor.author | Leem, Hyun Hee | - |
dc.contributor.author | Lee, Hyun-Shik | - |
dc.contributor.author | Lee, Hong Jun | - |
dc.contributor.author | Lee, Sang-Rae | - |
dc.contributor.author | Lee, Dong-Seok | - |
dc.date.accessioned | 2021-06-18T08:43:50Z | - |
dc.date.available | 2021-06-18T08:43:50Z | - |
dc.date.issued | 2017-08-01 | - |
dc.identifier.issn | 0031-7012 | - |
dc.identifier.issn | 1423-0313 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/45647 | - |
dc.description.abstract | Chrysophanic acid, or chrysophanol, is an anthraquinone found in Rheum palmatum, which was used in the preparation of oriental medicine in ancient China. The hippocampus plays a major role in controlling the activities of the short- and long-term memory. It is one of the major regions affected by excessive cell death in Alzheimer's disease. Therefore, neuronal cell-death modulation in the hippocampus is important for maintaining neuronal function. We investigated chrysophanol's effects on glutamate-induced hippocampal neuronal cell death. Chrysophanol reduced glutamate-induced cell death via suppression of proapoptotic factors and reactive oxygen species generation. Furthermore, it downregulated glutamate-induced mitochondrial fission by inhibiting dynamin-related protein 1 (Drp1) dephosphorylation. Thus, chrysophanol suppressed hippocampal neuronal cell death via inhibition of Drp1-dependent mitochondrial fission, and can be used as a therapeutic agent for treating neuronal cell death-mediated neurodegenerative diseases. (C) 2017 S. Karger AG, Basel | - |
dc.format.extent | 8 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | KARGER | - |
dc.title | Chrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission | - |
dc.type | Article | - |
dc.identifier.doi | 10.1159/000477814 | - |
dc.identifier.bibliographicCitation | PHARMACOLOGY, v.100, no.3-4, pp 153 - 160 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000407176000007 | - |
dc.identifier.scopusid | 2-s2.0-85021151963 | - |
dc.citation.endPage | 160 | - |
dc.citation.number | 3-4 | - |
dc.citation.startPage | 153 | - |
dc.citation.title | PHARMACOLOGY | - |
dc.citation.volume | 100 | - |
dc.type.docType | Article | - |
dc.publisher.location | 스위스 | - |
dc.subject.keywordAuthor | Chrysophanol | - |
dc.subject.keywordAuthor | Mitochondrial fission | - |
dc.subject.keywordAuthor | Dynamin-related protein 1 | - |
dc.subject.keywordAuthor | Reactive oxygen species | - |
dc.subject.keywordAuthor | Neuronal cell death | - |
dc.subject.keywordPlus | NEURODEGENERATIVE DISEASES | - |
dc.subject.keywordPlus | ALZHEIMERS-DISEASE | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | POWDERY MILDEW | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | DYSFUNCTION | - |
dc.subject.keywordPlus | DISORDERS | - |
dc.subject.keywordPlus | PHYSCION | - |
dc.subject.keywordPlus | INSIGHTS | - |
dc.subject.keywordPlus | NECROSIS | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.