Ecklonia cava-derived Polysaccharide Prevent Hydro Peroxide-induced Oxidative Stress and Neurotoxicity in Human Microglial HMO6 Cells

Yeon-Joo Lee¹, Ji-Hyun Hwang¹, Kui-Jin Kim^1, and Boo-Yong Lee^1,

¹Department of Food Science and Biotechnology, CHA University, Gyeonggi 463-400, South Korea

Cite this paper:
Yeon-Joo Lee, Ji-Hyun Hwang, Kui-Jin Kim and Boo-Yong Lee. Ecklonia cava-derived Polysaccharide Prevent Hydro Peroxide-induced Oxidative Stress and Neurotoxicity in Human Microglial HMO6 Cells. Journal of Food and Nutrition Research. 2017; 5(3):187-190. doi: 10.12691/jfnr-5-3-8

Abstract

In the present study, we examined the beneficial effect of Ecklonia cava-derived polysaccharide (ECAP), which is residual product after bioactive polyphenol isolation form Ecklonia cava, on neurotoxicity and oxidative stress in hydro peroxide-treated human microglia HMO6 cells. We sought that ECAP inhibited the expression of p53 and Bcl-2 in hydro peroxide-induced HMO6 cells. ECAP dramatically suppressed the cleaved form of caspase-3 in hydro peroxide-treated HMO6 cells. Moreover, we observed that hydro peroxide stimulated the expression of glucose-6-phosphate dehydrogenase (G6PDH) and its downstream target NADPH oxidase 4 (NOX4) in HMO6 cells. In contrast, ECAP suppressed the expression of G6PDH and NOX4 in hydro peroxide-treated HMO6 cells. We also observed that anti-oxidant enzymes including superoxide dismutase 1 (SOD1), superoxide dismutase 2 (SOD2), and catalase were stimulated by ECAP to protect the neurotoxicity in hydro peroxide-treated HMO6 cells. Taken together, we demonstrated that ECAP may inhibit hydro peroxide-mediated neurotoxicity through the regulation of p53 and Bcl-2 genes in HMO6 cells and ameliorate oxidative stress in hydro peroxide-treated HMO6 cells. Therefore we suggest that ECAP may hold the potential to prevent the incidence of neuronal damage-mediated neurodegenerative diseases.

Keywords:
Ecklonia cava seaweed polysaccharide neurotoxicity oxidative stress microglia HMO6 neuroprotection

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