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<records>
  <record>
    <language>eng</language>
    <publisher>Science and Education Publishing</publisher>
    <journalTitle>Journal of Food and Nutrition Research</journalTitle>
    <eissn>2333-1240</eissn>
    <publicationDate>2017-03-20</publicationDate>
    <volume>5</volume>
    <issue>3</issue>
    <startPage>187</startPage>
    <endPage>190</endPage>
    <doi>10.12691/jfnr-5-3-8</doi>
    <publisherRecordId>JFNR2017538</publisherRecordId>
    <documentType>article</documentType>
    <title language="eng">Ecklonia cava-derived Polysaccharide Prevent Hydro Peroxide-induced Oxidative Stress and Neurotoxicity in Human Microglial HMO6 Cells</title>
    <authors>
      <author>
        <name>Yeon-Joo Lee</name>
        <affiliationId>1</affiliationId>
      </author>
      <author>
        <name>Ji-Hyun Hwang</name>
        <affiliationId>1</affiliationId>
      </author>
      <author>
        <name>Kui-Jin Kim</name>
        <email>Kuijin.Kim@cha.ac.kr, bylee@cha.ac.kr</email>
        <affiliationId>1</affiliationId>
      </author>
      <author>
        <name>Boo-Yong Lee</name>
        <email>Kuijin.Kim@cha.ac.kr, bylee@cha.ac.kr</email>
        <affiliationId>1</affiliationId>
      </author>
    </authors>
    <affiliationsList>
      <affiliationName affiliationId="1">Department of Food Science and Biotechnology, CHA University, Gyeonggi 463-400, South Korea</affiliationName>
    </affiliationsList>
    <abstract language="eng">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>
    <fullTextUrl format="pdf">http://pubs.sciepub.com/jfnr/5/3/8/jfnr-5-3-8.pdf</fullTextUrl>
    <keywords language="eng">
      <keyword>Ecklonia cava</keyword>
      <keyword>seaweed</keyword>
      <keyword>polysaccharide</keyword>
      <keyword>neurotoxicity</keyword>
      <keyword>oxidative stress</keyword>
      <keyword>microglia</keyword>
      <keyword>HMO6</keyword>
      <keyword>neuroprotection</keyword>
    </keywords>
  </record>
</records>