1 Ocak 2021 Dergi makalesi Açık Erişim

Senol, Sefika Pinar; Temiz-Resitoglu, Meryem; Guden, Demet Sinem; Sari, Ayse Nihal; Sahan-Firat, Seyhan; Tunctan, Bahar

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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/231630</identifier>
  <creators>
    <creator>
      <creatorName>Senol, Sefika Pinar</creatorName>
      <givenName>Sefika Pinar</givenName>
      <familyName>Senol</familyName>
      <affiliation>Mersin Univ, Dept Pharmacol, Fac Pharm, Mersin, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Temiz-Resitoglu, Meryem</creatorName>
      <givenName>Meryem</givenName>
      <familyName>Temiz-Resitoglu</familyName>
      <affiliation>Mersin Univ, Dept Pharmacol, Fac Pharm, Mersin, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Guden, Demet Sinem</creatorName>
      <givenName>Demet Sinem</givenName>
      <familyName>Guden</familyName>
      <affiliation>Mersin Univ, Dept Pharmacol, Fac Pharm, Mersin, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Sari, Ayse Nihal</creatorName>
      <givenName>Ayse Nihal</givenName>
      <familyName>Sari</familyName>
      <affiliation>Mersin Univ, Dept Pharmacol, Fac Pharm, Mersin, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Sahan-Firat, Seyhan</creatorName>
      <givenName>Seyhan</givenName>
      <familyName>Sahan-Firat</familyName>
      <affiliation>Mersin Univ, Dept Pharmacol, Fac Pharm, Mersin, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Tunctan, Bahar</creatorName>
      <givenName>Bahar</givenName>
      <familyName>Tunctan</familyName>
      <affiliation>Mersin Univ, Dept Pharmacol, Fac Pharm, Mersin, Turkey</affiliation>
    </creator>
  </creators>
  <titles>
    <title>Suppression Of Tlr4/Myd88/Tak1/Nf-Kappa B/Cox-2 Signaling Pathway In The Central Nervous System By Bexarotene, A Selective Rxr Agonist, Prevents Hyperalgesia In The Lipopolysaccharide-Induced Pain Mouse Model</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2021</publicationYear>
  <dates>
    <date dateType="Issued">2021-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/231630</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1007/s11064-020-03197-7</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">A selective RXR agonist, bexarotene, has been shown to have anti-inflammatory, anti-nociceptive, and neuroprotective effects in several models of numerous neurological diseases characterized by systemic inflammation. The mechanisms underlying these effects remains unknown. To elucidate these mechanisms, we investigated whether the TLR4/MyD88/TAK1/NF-kappa B/COX-2 signaling pathway in the CNS mediates the effect of bexarotene to prevent hyperalgesia in the LPS-induced inflammatory pain mouse model. The reaction time to thermal stimuli within 30 s was evaluated by the hot plate test in male mice treated with saline, LPS (10 mg/kg), DMSO, and/or bexarotene (0.1, 1, 3, or 10 mg/kg) after 6 h. The latency to the thermal stimulus (18.11 +/- 1.36 s) in the LPS-treated mice was significantly decreased by 30% compared with saline-treated mice (25.84 +/- 1.99 s). Treatment with bexarotene only at a dose of 10 mg/kg showed a significant increase in the latency by 22.49 +/- 1.00 s compared with LPS-treated mice. Bexarotene also prevented the reduction in RXR alpha protein expression associated with a rise in the expression of TLR4, MyD88, phosphorylated TAK1, NF-kappa B p65, phosphorylated NF-kappa B p65, COX-2, and IL-1 beta proteins, in addition to COX-2 activity and levels of PGE(2) and IL-1 beta in the brains and spinal cords of the LPS-treated animals. Likely, decreased activity of TLR4/MyD88/TAK1/NF-kappa B/COX-2 signaling pathway in addition to increased pro-inflammatory cytokine formation in the CNS of mice participates in the protective effect of bexarotene against hyperalgesia induced by LPS.</description>
  </descriptions>
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