Acer okamotoanum inhibit the hydrogen peroxide-induced oxidative stress in c6 glial cells
- Authors
- Choi, S.Y.; Kim, J.H.; Quilantang, N.G.; Lee, S.; Cho, E.J.
- Issue Date
- Sep-2018
- Publisher
- Korean Society of Pharmacognosy
- Keywords
- Acer okamotoanum; Apoptosis; C6 glial cell; Inflammation; Reactive oxygen species
- Citation
- Natural Product Sciences, v.24, no.3, pp 148 - 154
- Pages
- 7
- Journal Title
- Natural Product Sciences
- Volume
- 24
- Number
- 3
- Start Page
- 148
- End Page
- 154
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/3276
- DOI
- 10.20307/nps.2018.24.3.148
- ISSN
- 1226-3907
- Abstract
- Chronic oxidative stress due to the accumulation of reactive oxygen species (ROS) in neuronal cells ultimately leads to neurodegenerative diseases. The use of natural therapies for the prevention of ROS-induced cell damage and for the treatment of neurodegenerative disorders has shown promising results. In this study, we evaluated the neuroprotective effects of the ethyl acetate (EtOAc) fraction of A. okamotoanum against the hydrogen peroxide (H2O2)-induced oxidative stress in C6 glial cells. Results show that cell viability was decreased in cells incubated with H2O2, whereas the addition of EtOAc fraction treatments in such cells significantly increased viability. The EtOAc fraction showed the highest inhibitory activity against ROS production and it also decreased the expressions of inflammatory proteins including cyclooxygenase-2, inducible nitric oxide synthase and interleukin-1β. Furthermore, the EtOAc fraction inhibited apoptosis by regulating the protein expressions cleaved caspase-9,-3, poly ADP ribose polymerase, Bax and Bcl-2. Therefore, these results show that the EtOAc fraction of A. Okamotoanum exhibits neuroprotective effects against H2O2 induced oxidative damage by regulating the inflammatory reaction and apoptotic pathway. © 2018, Korean Society of Pharmacognosy. All rights reserved.
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