Morin Attenuates Diclofenac-Induced Hepatocellular Death Injury via Nrf2/Ho-1/NQO1, Beclin-1/LC3A/LC3B and p53/Bax/Caspase Signalling Pathways

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dc.authorid0000-0001-6775-7858
dc.authorid0000-0002-8222-5515
dc.authorid0000-0002-4581-4492
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorŞimşek, Hasan
dc.contributor.authorGür, Cihan
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2025-07-23T08:07:59Z
dc.date.available2025-07-23T08:07:59Z
dc.date.issued2025
dc.departmentTıp Fakültesi
dc.description.abstractDiclofenac (DF), a nonsteroidal and anti-inflammatory drug, has limited use due to its adverse effects on the liver. On the other hand, morin, a bioflavonoid, has biological and pharmacological properties. This study aims to investigate whether morin may protect against diclofenac-induced liver toxicity. For this purpose, morin (50 or 100 mg/kg) treatment was given orally to the rats for 5 days, and DF (50 mg/kg) was administered intraperitoneally on the 4th and 5th days of the study. Molecular, biochemical, immunohistochemical and histological methods were used to investigate cyclooxygenase enzymes, oxidative stress, apoptosis and autophagy in liver tissue. According to the data obtained, it was observed that DF caused oxidative stress, autophagy and apoptosis damage in liver tissues. Morin showed antioxidant properties, causing a decrease in MDA in hepatic tissue, an increase in the activities of endogenous antioxidants (glutathione peroxidase, superoxide dismutase and catalase) and GSH, HO-1, Nrf2 and NQO1 mRNA levels. Moreover, morin reversed the changes in the levels of apoptotic and autophagic parameters such as bax, bcl-2, cytochrome c, p53, Apaf-1, caspase-3, caspase-6, caspase-9, beclin-1, LC3A, LC3B, MAPK14, MAP15, JNK. When the histopathological analysis results were examined, degenerative changes occurred in the livers of rats administered DF, while morin administration showed a morphological structure close to the control group. As a result, it was determined that oxidative stress, autophagy and apoptosis caused by DF were suppressed by morin, thus protecting the liver tissue from damage.
dc.identifier.doi10.1002/jbt.70372
dc.identifier.issn10956670
dc.identifier.issue7
dc.identifier.pmid40551516
dc.identifier.scopus2-s2.0-105009578798
dc.identifier.urihttps://dx.doi.org/10.1002/jbt.70372
dc.identifier.urihttps://hdl.handle.net/20.500.12451/13533
dc.identifier.volume39
dc.identifier.wosWOS:001513602800001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakPubMed
dc.indekslendigikaynakScopus
dc.indekslendigikaynakWeb of Science
dc.institutionauthorAkaras, Nurhan
dc.institutionauthorŞimşek, Hasan
dc.institutionauthorKandemir, Fatih Mehmet
dc.institutionauthorid0000-0002-8457-9448
dc.institutionauthorid0000-0001-5573-4923
dc.institutionauthorid0000-0002-8490-2479
dc.language.isoen
dc.publisherJohn Wiley and Sons Inc
dc.relation.ispartofJournal of Biochemical and Molecular Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectApoptosis
dc.subjectAutophagy
dc.subjectDiclofenac
dc.subjectLiver
dc.subjectMorin
dc.subjectOxidative Stress
dc.titleMorin Attenuates Diclofenac-Induced Hepatocellular Death Injury via Nrf2/Ho-1/NQO1, Beclin-1/LC3A/LC3B and p53/Bax/Caspase Signalling Pathways
dc.typeArticle

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