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    <subfield code="a">10.1111/apha.12498</subfield>
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    <subfield code="2">sideral</subfield>
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    <subfield code="a">ART-2015-99902</subfield>
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    <subfield code="a">eng</subfield>
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  <datafield tag="100" ind1=" " ind2=" ">
    <subfield code="a">Latorre, E.</subfield>
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  <datafield tag="245" ind1=" " ind2=" ">
    <subfield code="a">Oxidative stress balance between pro- and anti-inflammatory factors in human intestinal epithelial cells</subfield>
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  <datafield tag="260" ind1=" " ind2=" ">
    <subfield code="c">2015</subfield>
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    <subfield code="a">Access copy available to the general public</subfield>
    <subfield code="f">Unrestricted</subfield>
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    <subfield code="a">Background: Oxidative stress plays a key role in the development of intestinal inflammatory diseases. Several pro-inflammatory mediators may generate oxidation products that exacerbate the inflammatory damage. Gastrointestinal molecules, like serotonin (5- HT), adenosine and melatonin, which are involved in intestinal physiology, have also been described as intestinal pro-inflammatory factors; whereas IL-10, a known anti-inflammatory cytokine, has also been implicated in intestinal pathophysiology. Aim: The aim of this study was to analyze the contribution of pro-inflammatory and anti-inflammatory molecules to oxidative stress balance, as well as to assess their effect on cellular antioxidant enzymes activity, in intestinal epithelial cells. Methods: Caco-2 cells were treated with the different molecules, and the oxidative stress was determined by measuring lipid peroxidation (MDA+4HDA) and protein carbonyl levels. The activity of the anti-oxidant enzymes (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) was also analyzed in treated cells. Results: Pro-inflammatory factors (5-HT, adenosine, melatonin and TNFa) increased oxidative damage in both lipids and proteins. Theses molecules, except melatonin, also inhibited the activity of antioxidant enzymes. With regard to IL-10, this cytokine was not shown to alter cellular oxidative damage, but was able to reduce the oxidative damage g by pro-inflamatory factors, and to restore their effects on anti-oxidant enxymes activities. Unexpectedly, IL-10, together with melatonin, was found to increase the antioxidant activity above the control. Conclusions: The anti-oxidant effect of IL-10 emphasizes the role of this cytokine as a potential therapy for the treatment of intestinal inflammation induced by pro-inflammatory molecules.</subfield>
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    <subfield code="9">info:eu-repo/grantAgreement/ES/DGA/ARAINF-012-2008</subfield>
    <subfield code="9">info:eu-repo/grantAgreement/ES/DGA/B022-13</subfield>
    <subfield code="9">info:eu-repo/grantAgreement/ES/DGA/B105-11</subfield>
    <subfield code="9">info:eu-repo/grantAgreement/ES/DGA/B61</subfield>
    <subfield code="9">info:eu-repo/grantAgreement/ES/MICINN-FEDER/BFU2009-08149</subfield>
    <subfield code="9">info:eu-repo/grantAgreement/ES/MICINN-FEDER/BFU2010-18971</subfield>
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    <subfield code="9">info:eu-repo/semantics/openAccess</subfield>
    <subfield code="a">by</subfield>
    <subfield code="u">http://creativecommons.org/licenses/by/3.0/es/</subfield>
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    <subfield code="a">4.066</subfield>
    <subfield code="b">2015</subfield>
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    <subfield code="a">PHYSIOLOGY</subfield>
    <subfield code="b">13 / 83 = 0.157</subfield>
    <subfield code="c">2015</subfield>
    <subfield code="d">Q1</subfield>
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    <subfield code="a">1.654</subfield>
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  <datafield tag="593" ind1=" " ind2=" ">
    <subfield code="a">Physiology</subfield>
    <subfield code="c">2015</subfield>
    <subfield code="d">Q1</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Layunta, E.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0001-5573-6144</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Gimeno, A.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0003-2373-6056</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Grasa, L.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0002-5306-9365</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Castro, M.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0001-8584-3979</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">García, S.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0003-3970-5457</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Gros, B.</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Arruebo, M.P.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0002-2114-0577</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Alcalde, A.I.</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Mesonero, J.E.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0003-4758-3998</subfield>
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  <datafield tag="710" ind1="2" ind2=" ">
    <subfield code="1">1005</subfield>
    <subfield code="2">410</subfield>
    <subfield code="a">Universidad de Zaragoza</subfield>
    <subfield code="b">Dpto. Farmacología y Fisiolog.</subfield>
    <subfield code="c">Área Fisiología</subfield>
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  <datafield tag="710" ind1="2" ind2=" ">
    <subfield code="1">1007</subfield>
    <subfield code="2">610</subfield>
    <subfield code="a">Universidad de Zaragoza</subfield>
    <subfield code="b">Dpto. Medicina, Psiqu. y Derm.</subfield>
    <subfield code="c">Area Medicina</subfield>
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  <datafield tag="773" ind1=" " ind2=" ">
    <subfield code="g">214, Suppl. 701 (2015), 30 [14]</subfield>
    <subfield code="p">Acta Physiol.</subfield>
    <subfield code="t">Acta Physiologica</subfield>
    <subfield code="x">1748-1708</subfield>
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