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<!DOCTYPE ArticleSet PUBLIC "-//NLM//DTD PubMed 2.0//EN" "http://www.ncbi.nlm.nih.gov:80/entrez/query/static/PubMed.dtd">
<ArticleSet>
<Article>
<Journal>
<PublisherName>Science and Education Publishing</PublisherName>
<JournalTitle>Journal of Food and Nutrition Research</JournalTitle>
<Issn>2333-1240</Issn>
<Volume>5</Volume>
<Issue>3</Issue>
<PubDate PubStatus="epublish">
<Year>2017</Year>
<Month>3</Month>
<Day>20</Day>
</PubDate>
</Journal>
<ArticleTitle>Ecklonia cava-derived Polysaccharide Prevent Hydro Peroxide-induced Oxidative Stress and Neurotoxicity in Human Microglial HMO6 Cells</ArticleTitle>
<FirstPage>187</FirstPage>
<LastPage>190</LastPage>
<Language>EN</Language>
<AuthorList>
<Author>
<FirstName>Yeon-Joo</FirstName>
<LastName>Lee</LastName>
</Author>
<Author>
<FirstName>Ji-Hyun</FirstName>
<LastName>Hwang</LastName>
</Author>
<Author>
<FirstName>Kui-Jin</FirstName>
<LastName>Kim</LastName>
<Affiliation>Department of Food Science and Biotechnology, CHA University, Gyeonggi 463-400, South Korea</Affiliation>
</Author>
<Author>
<FirstName>Boo-Yong</FirstName>
<LastName>Lee</LastName>
<Affiliation>Department of Food Science and Biotechnology, CHA University, Gyeonggi 463-400, South Korea</Affiliation>
</Author>

</AuthorList>
<ArticleIdList>
<ArticleId IdType="pii">JFNR2017538</ArticleId>
<ArticleId IdType="doi">10.12691/jfnr-5-3-8</ArticleId>
</ArticleIdList>
<History>
<PubDate PubStatus="received">
<Year>2016</Year>
<Month>10</Month>
<Day>10</Day>
</PubDate>
<PubDate PubStatus="revised">
<Year>2017</Year>
<Month>1</Month>
<Day>4</Day>
</PubDate>
<PubDate PubStatus="accepted">
<Year>2017</Year>
<Month>3</Month>
<Day>18</Day>
</PubDate>
</History>
<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.</Abstract>
</Article>
</ArticleSet>
