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Chrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission

Authors
Chae, UnbinMin, Ju-SikLeem, Hyun HeeLee, Hyun-ShikLee, Hong JunLee, Sang-RaeLee, Dong-Seok
Issue Date
1-Aug-2017
Publisher
KARGER
Keywords
Chrysophanol; Mitochondrial fission; Dynamin-related protein 1; Reactive oxygen species; Neuronal cell death
Citation
PHARMACOLOGY, v.100, no.3-4, pp 153 - 160
Pages
8
Journal Title
PHARMACOLOGY
Volume
100
Number
3-4
Start Page
153
End Page
160
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/45647
DOI
10.1159/000477814
ISSN
0031-7012
1423-0313
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
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