Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats

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dc.authorid0000-0001-5608-554X
dc.contributor.authorVarışlı, Behçet
dc.contributor.authorÇağlayan, Cüneyt
dc.contributor.authorKandemir, Fatih Mehmet
dc.contributor.authorGür, Cihan
dc.contributor.authorAyna, Adnan
dc.contributor.authorAyna, Adnan
dc.contributor.authorGenç, Aydın
dc.contributor.authorTaysı, Seyithan
dc.date.accessioned2023-01-16T07:46:06Z
dc.date.available2023-01-16T07:46:06Z
dc.date.issued2023
dc.departmentTıp Fakültesi
dc.description.abstractDiclofenac (DF) is a non-steroidal anti-inflammatory drug (NSAID) generally prescribed for the treatment of pain. In spite of the widespread use of DF, hepatotoxicity has been reported after its administration. The current study discloses new evidence as regards of the curative effects of chrysin (CHR) on DF-induced hepatotoxicity by regulating oxidative stress, apoptosis, autophagy, and endoplasmic reticulum (ER) stress. Methods: The animals were separated into five different groups. Group-I was in control. Group-II received CHR-only (50 mg/kg bw, p.o.) on all 5 days. Group-III received DF-only (50 mg/kg bw, i.p.) on 4th and 5th day. Group-IV received DF (50 mg/kg bw) + CHR (25 mg/kg, bw) and group-V received DF (50 mg/kg, bw) + CHR (50 mg/kg, bw) for 5 days. Results: DF injection was associated with increased MDA while reduced GSH level, activities of superoxide dismutase, glutathione peroxidase, and catalase and mRNA levels of HO-1 and Nrf2 in the liver. DF injection caused apoptosis and autophagy in the liver by up-regulating caspase-3, Bax, LC3A, and LC3B levels and down-regulating Bcl-2. DF also caused ER stress by increasing mRNA transcript levels of ATF-6, IRE1, PERK, and GRP78. Additionally, it was observed that DF administration up-regulated MMP2 and MMP9. However, treatment with CHR at a dose of 25 and 50 mg/kg considerably ameliorated oxidative stress, apoptosis, autophagy, and ER stress in liver tissue. Conclusion: Overall, the data of this study indicate that liver damage associated with DF toxicity could be ameliorated by CHR administration.
dc.identifier.doi10.1007/s11033-022-07928-7
dc.identifier.issn0301-4851
dc.identifier.pmid36344803
dc.identifier.scopusqualityQ2
dc.identifier.urihttps:/dx.doi.org/10.1007/s11033-022-07928-7
dc.identifier.urihttps://hdl.handle.net/20.500.12451/9934
dc.identifier.wosWOS:000879677600002
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer Science and Business Media B.V.
dc.relation.ispartofMolecular Biology Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectApoptosis
dc.subjectAutophagy
dc.subjectChrysin
dc.subjectDiclofenac
dc.subjectEndoplasmic Reticulum Stress
dc.titleChrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats
dc.typeArticle

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