Chrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission
- Authors
- Chae, Unbin; Min, Ju-Sik; Leem, Hyun Hee; Lee, Hyun-Shik; Lee, Hong Jun; Lee, Sang-Rae; Lee, 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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