AGK2, a SIRT2 inhibitor, ameliorates D-galactose-induced liver fibrosis by inhibiting fibrogenic factors

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dc.authoridSONUGUR, FATMA GIZEM/0000-0002-2773-2872
dc.contributor.authorBahar, Asli Nur
dc.contributor.authorKeskin-Aktan, Arzu
dc.contributor.authorAkarca-Dizakar, Saadet Ozen
dc.contributor.authorSonugur, Gizem
dc.contributor.authorAkbulut, Kazime Gonca
dc.date.accessioned2025-03-20T09:51:25Z
dc.date.available2025-03-20T09:51:25Z
dc.date.issued2024
dc.departmentİzmir Bakırçay Üniversitesi
dc.description.abstractIn our study, we aimed to investigate the effect of SIRT2 inhibition on function, fibrosis and inflammation in liver fibrosis induced by D-Galactose (D-Gal) administration. A total of 32 3-month-old Sprague Dawley rats were used in the study. Rats were divided into 4 groups as Control, d-Gal, Solvent+d-Gal, d-Gal+AGK2+Solvent. d-Gal (150 mg/kg/day), AGK-2 (10 mu M/bw) as a specific SIRT2 inhibitor, 4%DMSO + PBS as a solvent was applied to the experimental groups and physiological saline was applied to the control group for 10 weeks. All applications were performed subcutaneously. Histological fibrotic changes were studied in the liver tissues by Masson's trichrome staining, hematoxylin and eosin staining and immunohistochemistry and the levels of selected factors were determined by quantitative reverse transcription-polymerase chain reaction, western blot analysis, and immunohistochemical analysis. Biochemical parameters and Paraoxonase levels were determined in the plasma. d-Galactose administration increased AST, AST-ALT Ratio, APRI, SIRT2 protein expression, IL1 beta, TGF beta, beta-catenin, Type I collagen, Type III collagen and alpha-SMA, collagen fiber density and histopathological score. ALT and lipid panels were not changed and paraxonase plasma level was shown to decrease. These effects were largely blocked by the SIRT2 inhibitor AGK2. These findings suggest that SIRT2 inhibition attenuates d-Gal-induced liver injury and that this protection may be due to its antifibrotic and anti-inflammatory activities.
dc.description.sponsorshipTurkiye Bilimsel ve Teknolojik Arastirma Kurumu
dc.description.sponsorshipTurkiye Bilimsel ve Teknolojik Arastirma Kurumu
dc.identifier.doi10.1002/jbt.70000
dc.identifier.issn1095-6670
dc.identifier.issn1099-0461
dc.identifier.issue11
dc.identifier.pmid39400930
dc.identifier.scopus2-s2.0-85206276039
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1002/jbt.70000
dc.identifier.urihttps://hdl.handle.net/20.500.14034/2538
dc.identifier.volume38
dc.identifier.wosWOS:001336718500001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofJournal of Biochemical and Molecular Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250319
dc.subjectd-Galactose
dc.subjectliver fibrosis
dc.subjectSIRT2 inhibition
dc.subjectTGF beta
dc.subjectbeta-catenin
dc.titleAGK2, a SIRT2 inhibitor, ameliorates D-galactose-induced liver fibrosis by inhibiting fibrogenic factors
dc.typeArticle

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