Morin ameliorates methotrexate-induced hepatotoxicity via targeting Nrf2/HO-1 and Bax/Bcl2/Caspase-3 signaling pathways

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dc.authoridKUCUKLER, Sefa/0000-0002-8222-5515
dc.authoridKANDEMIR, Fatih Mehmet/0000-0002-8490-2479
dc.contributor.authorKizil, Hamit Emre
dc.contributor.authorCaglayan, Cuneyt
dc.contributor.authorDarendelioglu, Ekrem
dc.contributor.authorAyna, Adnan
dc.contributor.authorGur, Cihan
dc.contributor.authorKandemir, Fatih Mehmet
dc.contributor.authorKucukler, Sefa
dc.date.accessioned2024-10-04T18:52:30Z
dc.date.available2024-10-04T18:52:30Z
dc.date.issued2023
dc.departmentBayburt Üniversitesien_US
dc.description.abstractBackgroundOrgan toxicity limits the therapeutic efficacy of methotrexate (MTX), an anti-metabolite therapeutic that is frequently used as an anti-cancer and immunosuppressive medicine. Hepatocellular toxicity is among the most severe side effects of long-term MTX use. The present study unveils new confirmations as regards the remedial effects of morin on MTX-induced hepatocellular injury through regulation of oxidative stress, apoptosis and MAPK signaling.Methods and resultsRats were subjected to oral treatment of morin (50 and 100 mg/kg body weight) for 10 days. Hepatotoxicity was induced by single intraperitoneal injection of MTX (20 mg/kg body weight) on the 5th day. MTX related hepatic injury was associated with increased MDA while decreased GSH levels, the activities of endogen antioxidants (glutathione peroxidase, superoxide dismutase and catalase) and mRNA levels of HO-1 and Nrf2 in the hepatic tissue. MTX treatment also resulted in apoptosis in the liver tissue via increasing mRNA transcript levels of Bax, caspase-3, Apaf-1 and downregulation of Bcl-2. Conversely, treatment with morin at different doses (50 and 100 mg/kg) considerably mitigated MTX-induced oxidative stress and apoptosis in the liver tissue. Morin also mitigated MTX-induced increases of ALT, ALP and AST levels, downregulated mRNA expressions of matrix metalloproteinases (MMP-2 and MMP-9), MAPK14 and MAPK15, JNK, Akt2 and FOXO1 genes.ConclusionAccording to the findings of this study, morin may be a potential way to shield the liver tissue from the oxidative damage and apoptosis.en_US
dc.identifier.doi10.1007/s11033-023-08286-8
dc.identifier.endpage3488en_US
dc.identifier.issn0301-4851
dc.identifier.issn1573-4978
dc.identifier.issue4en_US
dc.identifier.pmid36781607en_US
dc.identifier.scopus2-s2.0-85147998122en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage3479en_US
dc.identifier.urihttps://doi.org/10.1007/s11033-023-08286-8
dc.identifier.urihttp://hdl.handle.net/20.500.12403/3505
dc.identifier.volume50en_US
dc.identifier.wosWOS:000930317000003en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular Biology Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApoptosisen_US
dc.subjectHepatotoxicityen_US
dc.subjectMethotrexateen_US
dc.subjectMorinen_US
dc.subjectOxidative stressen_US
dc.titleMorin ameliorates methotrexate-induced hepatotoxicity via targeting Nrf2/HO-1 and Bax/Bcl2/Caspase-3 signaling pathwaysen_US
dc.typeArticleen_US

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