Pyroptosis and necroptosis inhibitor necrosulfonamide ameliorates lipopolysaccharide-induced inflammatory hyperalgesia in mice

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dc.authoridTUNCTAN, BAHAR/0000-0003-3439-7803
dc.authoridBAHCELI, OMER/0000-0002-5307-5976
dc.contributor.authorOzgen, Beyza
dc.contributor.authorSenol, Sefika Pinar
dc.contributor.authorYilmaz, Dilsah Ezgi
dc.contributor.authorTemiz-Resitoglu, Meryem
dc.contributor.authorBahceli, Omer
dc.contributor.authorTunctan, Bahar
dc.date.accessioned2025-03-17T12:25:11Z
dc.date.available2025-03-17T12:25:11Z
dc.date.issued2023
dc.departmentTarsus Üniversitesi
dc.description.abstractObjectives: This study aimed to investigate the effect of the gasdermin D (GSDMD) and mixed lineage kinase domain-like pseudokinase (MLKL) inhibitor, necrosulfonamide (NSA), on lipopolysaccharide (LPS)-induced hyperalgesia in mice. Methods: Reaction time to a thermal stimulus within 30 seconds was measured in male mice injected with saline, LPS, and/or NSA after 6 hours using the hot plate test. Immunoblotting studies were performed to determine changes in caspase-11/GSDMD-mediated pyroptosis, receptor-interacting serine/threonine-protein kinase (RIPK) 1/RIPK3/MLKL necrosome-mediated necroptosis, demyelination, and remyelination in the brains and spinal cords of animals. Results: NSA demonstrated significant antinociceptive activity compared with LPS-treated mice. In the tissues of LPS-treated mice, NSA decreased expression of caspase-11 p20, p30-GSDMD, interleukin-1 beta, high-mobility-group-box 1, and semaphorin 3A, and activity of RIPK1, RIPK3, and MLKL. NSA also increased the expression of myelin proteolipid protein. Conclusion: Therefore, NSA may have therapeutic potential in the treatment of inflammatory painful conditions due to bacterial infections.
dc.description.sponsorshipResearch Fund of Mersin University in Turkiye [2021-1-TP2-4393]
dc.description.sponsorshipThis study was supported by the Research Fund of Mersin University in Turkiye with Project Number 2021-1-TP2-4393. The findings of this work were included in the Master's Thesis of Pharm. M.S. Beyza Ozgen.
dc.identifier.doi10.3897/pharmacia.70.e108995
dc.identifier.endpage1354
dc.identifier.issn0428-0296
dc.identifier.issn2603-557X
dc.identifier.issue4
dc.identifier.scopus2-s2.0-85180784170
dc.identifier.scopusqualityQ2
dc.identifier.startpage1345
dc.identifier.urihttps://doi.org/10.3897/pharmacia.70.e108995
dc.identifier.urihttps://hdl.handle.net/20.500.13099/1540
dc.identifier.volume70
dc.identifier.wosWOS:001163466700002
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherPensoft Publishers
dc.relation.ispartofPharmacia
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250316
dc.subjectInflammatory hyperalgesia
dc.subjectlipopolysaccharide
dc.subjectnecroptosis
dc.subjectpyroptosis
dc.subjectnecrosulfonamide
dc.titlePyroptosis and necroptosis inhibitor necrosulfonamide ameliorates lipopolysaccharide-induced inflammatory hyperalgesia in mice
dc.typeArticle

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