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http://dx.doi.org/10.20307/nps.2018.24.3.148

Acer okamotoanum Inhibit the Hydrogen Peroxide-Induced Oxidative Stress in C6 Glial Cells  

Choi, Soo Yeon (Department of Food Science and Nutrition & Kimchi Research Institute, Pusan National University)
Kim, Ji Hyun (Department of Food Science and Nutrition & Kimchi Research Institute, Pusan National University)
Quilantang, Norman G. (Department of Integrative Plant Science, Chung-Ang University)
Lee, Sanghyun (Department of Integrative Plant Science, Chung-Ang University)
Cho, Eun Ju (Department of Food Science and Nutrition & Kimchi Research Institute, Pusan National University)
Publication Information
Natural Product Sciences / v.24, no.3, 2018 , pp. 148-154 More about this Journal
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 ($H_2O_2$)-induced oxidative stress in C6 glial cells. Results show that cell viability was decreased in cells incubated with $H_2O_2$, 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-$1{\beta}$. 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 $H_2O_2$ induced oxidative damage by regulating the inflammatory reaction and apoptotic pathway.
Keywords
Acer okamotoanum; C6 glial cell; Inflammation; Apoptosis; Reactive oxygen species;
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