1 Ocak 2014 Dergi makalesi Açık Erişim

Bayrakdar, E. Turunc; Uyanikgil, Y.; Kanit, L.; Koylu, E.; Yalcin, A.

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/61321</identifier>
  <creators>
    <creator>
      <creatorName>Bayrakdar, E. Turunc</creatorName>
      <givenName>E. Turunc</givenName>
      <familyName>Bayrakdar</familyName>
      <affiliation>Ege Univ, Fac Pharm, Dept Biochem, TR-35100 Izmir, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Uyanikgil, Y.</creatorName>
      <givenName>Y.</givenName>
      <familyName>Uyanikgil</familyName>
      <affiliation>Ege Univ, Fac Med, Dept Histol &amp; Embryol, TR-35100 Izmir, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Kanit, L.</creatorName>
      <givenName>L.</givenName>
      <familyName>Kanit</familyName>
    </creator>
    <creator>
      <creatorName>Koylu, E.</creatorName>
      <givenName>E.</givenName>
      <familyName>Koylu</familyName>
    </creator>
    <creator>
      <creatorName>Yalcin, A.</creatorName>
      <givenName>A.</givenName>
      <familyName>Yalcin</familyName>
    </creator>
  </creators>
  <titles>
    <title>Nicotinamide Treatment Reduces The Levels Of Oxidative Stress, Apoptosis, And Parp-1 Activity In A Beta (1-42)-Induced Rat Model Of Alzheimer'S Disease</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2014</publicationYear>
  <dates>
    <date dateType="Issued">2014-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/61321</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.3109/10715762.2013.857018</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">The underlying mechanisms of Alzheimer's Disease (AD) are still unclear. It is suggested that poly(ADP-ribose) polymerase-1(PARP-1) overactivation can cause neuroinflammation and cell death. In this study we searched the effects of nicotinamide(NA), endogenous PARP-1 inhibitor, on oxidative stress, apoptosis, and the regulation of PARP-1 and nuclear factor kappa B(NF-kappa B) in amyloid beta peptide(1-42)(A beta(1-42))-induced neurodegeneration. Sprague-Dawley rats were divided into four groups as control, A beta(1-42), A beta(1-42) + NA(100 and 500 mg/kg). All groups were stereotaxically injected bilaterally into the hippocampus with A beta(1-42) or saline. After surgery NA administrations were made intraperitoneally(ip) for 7 days. In order to investigate the effects of A beta(1-42) and NA, protein carbonyls, lipid peroxidation, reactive oxygen species(ROS) production, glutathione(GSH) levels, activities of antioxidant enzymes(catalase, superoxide dismutase, glutathione peroxidase), mitochondrial function, mRNA and protein levels of PARP-1, NF-kappa B, p53, Bax, and Bcl-2 were measured in specific brain regions such as cortex and hippocampus. A beta(1-42) treatment only increased the oxidative stress parameters and caused decline in antioxidant enzyme activities, mitochondrial function, and GSH levels. Also, overexpression of PARP-1, NF-kappa B, p53, Bax, and the decreased levels of Bcl-2 were observed in A beta(1-42)-treated group. NA treatments against A beta(1-42)-upregulated Bcl-2 and downregulated PARP-1, NF-kappa B, p53, and Bax levels. NA treatments also decreased the oxidative stress parameters and elevated antioxidant enzyme activities, GSH levels, and mitochondrial function against A beta(1-42) treatment. These data suggest that NA may have a therapeutic potential in neurodegenerative processes due to the decreased levels of oxidative stress, apoptosis, and PARP-1 activity.</description>
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