NLRX1 ligand, docosahexaenoic acid, ameliorates LPS-induced inflammatory hyperalgesia by decreasing TRAF6/IKK/IκB-α/NF-κB signaling pathway activity

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dc.contributor.authorYilmaz, Dilsah Ezgi
dc.contributor.authorSenol, Sefika Pinar
dc.contributor.authorTemiz-Resitoglu, Meryem
dc.contributor.authorSahan-Firat, Seyhan
dc.contributor.authorTunctan, Bahar
dc.date.accessioned2025-03-17T12:25:32Z
dc.date.available2025-03-17T12:25:32Z
dc.date.issued2023
dc.departmentTarsus Üniversitesi
dc.description.abstractThe nucleotide-binding oligomerization domain-like receptor X1 (NLRX1) has been associated with various anti-inflammatory mechanisms. We investigated whether the NLRX1 ligand docosahexaenoic acid (DHA) ameliorates lipopolysaccharide (LPS)-induced inflammatory hyperalgesia by interacting with tumor necrosis factor receptor-associated factor 6 (TRAF6)/inhibitor of KB (IKB) kinase (IKK)/IKB-alpha/nuclear factor-KB (NF -KB) signaling pathway in the central nervous system. Reaction time to thermal stimuli within 30 seconds was measured in male mice injected with saline, lipopolysaccharide (LPS), and/or DHA after 6 hours using the hot plate test. Co-immunoprecipitation and immunoblotting studies were performed to determine the activation of the TRAF6/IKK/IKB-alpha/NF-KB pathway in the brains and spinal cords of animals. Latency to the thermal stimulus was reduced by 30% in LPS-injected endotoxemic mice compared with saline-injected mice. Treatment with DHA significantly improved latency compared with endotoxemic mice. In the brain and spinal cord of LPS-injected mice, treatment with DHA also prevented the increase in the expression and/or activity of (1) IKK alpha/IKK beta, IKK gamma, and K63 U in the NLRX1-immunoprecipitated tissues, (2) IKK alpha/IKK beta, K63 U, and K48 U in the IKK gamma-immunoprecipitated tissues, and (3) IKB-alpha, NF-KB p65, and interleukin-1 beta associated with decreased IKB-alpha expression. These findings suggest that inhibition of IKK/IKB-alpha/NF-KB signaling by dissociation of NLRX1 from TRAF6 in response to LPS treatment contributes to the protective effect of DHA against inflammatory hyperalgesia.
dc.description.sponsorshipMersin University [2019-3-TP3-3773]; Scientific and Technological Research Council of Turkey [SBAG-219S353]
dc.description.sponsorshipThis work was supported by grants from Mersin University for 2019-3-TP3-3773 and The Scientific and Technological Research Council of Turkey for SBAG-219S353.
dc.identifier.doi10.14715/cmb/2023.69.9.3
dc.identifier.endpage23
dc.identifier.issn0145-5680
dc.identifier.issn1165-158X
dc.identifier.issue9
dc.identifier.pmid37807339
dc.identifier.scopus2-s2.0-85175433706
dc.identifier.scopusqualityQ4
dc.identifier.startpage15
dc.identifier.urihttps://doi.org/10.14715/cmb/2023.69.9.3
dc.identifier.urihttps://hdl.handle.net/20.500.13099/1716
dc.identifier.volume69
dc.identifier.wosWOS:001116557900003
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherC M B Assoc
dc.relation.ispartofCellular and Molecular Biology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250316
dc.subjectDocosahexaenoic acid
dc.subjectinflammatory hyperalgesia
dc.subjectlipopoly-saccharide
dc.subjectNLRX1
dc.subjectTRAF6/IKK/ I kappa B-alpha/NF-kappa B signaling pathway
dc.titleNLRX1 ligand, docosahexaenoic acid, ameliorates LPS-induced inflammatory hyperalgesia by decreasing TRAF6/IKK/IκB-α/NF-κB signaling pathway activity
dc.typeArticle

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