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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<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Senol, Sefika Pinar</dc:creator>
  <dc:creator>Temiz-Resitoglu, Meryem</dc:creator>
  <dc:creator>Guden, Demet Sinem</dc:creator>
  <dc:creator>Sari, Ayse Nihal</dc:creator>
  <dc:creator>Sahan-Firat, Seyhan</dc:creator>
  <dc:creator>Tunctan, Bahar</dc:creator>
  <dc:date>2021-01-01</dc:date>
  <dc:description>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.</dc:description>
  <dc:identifier>https://aperta.ulakbim.gov.trrecord/231630</dc:identifier>
  <dc:identifier>oai:aperta.ulakbim.gov.tr:231630</dc:identifier>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights>
  <dc:source>NEUROCHEMICAL RESEARCH 46(3) 624-637</dc:source>
  <dc: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</dc:title>
  <dc:type>info:eu-repo/semantics/article</dc:type>
  <dc:type>publication-article</dc:type>
</oai_dc:dc>