Galangin Protects AML-12 Cells Against Dactinomycin Induced Hepatotoxicity

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dc.authoridOltulu, Cagatay/0000-0002-6051-3479
dc.authorwosidYakut, Zatiye Ayça Çevikelli/ACP-2487-2022
dc.authorwosidOltulu, Cagatay/V-1823-2018
dc.contributor.authorAkinci, Melek
dc.contributor.authorOltulu, Cagatay
dc.contributor.authorBakar, Elvan
dc.contributor.authorCevikelli Yakut, Zatiye Ayca
dc.date.accessioned2024-06-12T10:59:08Z
dc.date.available2024-06-12T10:59:08Z
dc.date.issued2023
dc.departmentTrakya Üniversitesien_US
dc.description.abstractAim: The purpose of this study was to evaluate the effects of galangin (Gal) on dactinomycin induced hepatotoxicity in vitro. Materials and Methods: AML -12 cell line was divided into 4 groups as the control, Gal, dactinomycin, and Gal+dactinomycin groups. IC50 dose was determined by the thiazolyl blue tetrazolium bromide test. Gene expressions of glutathione (GSH), superoxide dismutase (SOD), catalase, caspase 3 (Cas-3), Cas-9, apoptotic protease activating factor -1 (Apaf-1), B cell CLL/lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), tumor protein p53 (p53), second mitochondria -derived activator of caspase/direct inhibitor of apoptosis-binding protein (smac/DIABLO), topoisomerase (Top) I, and Top II were determined with quantitative real-time polymerase chain reaction analysis. Results: Dactinomycin elevated the expression of SOD, catalase, and GSH in response to oxidative effects. In the Gal+dactinomycin group, Gal administration reduced Apaf-1 expression and increased Bcl-2 expression with antiapoptotic effects. In the dactinomycin group, p53 levels increased due to the defense mechanism against DNA damage. Gal increased smac/DIABLO expression to remove damaged structures. Bcl-2 and smac/DIABLO expression levels in the groups were inversely proportional. In the Gal+dactinomycin group, Top II expression level was lower than in the dactinomycin group. This result indicated that double strand of DNA damage was diminished by Gal. Conclusion: Gal protected against the hepatotoxicity due to dactinomycin with antioxidant and antiapoptotic effects. Further experimental studies are needed to establish the use of Gal in liver damage.en_US
dc.description.sponsorshipTrakya University Scientific Research Projects Committee [2018/274]en_US
dc.description.sponsorshipFinancial Disclosure: This study was funded by Trakya University Scientific Research Projects Committee with grant number 2018/274.en_US
dc.identifier.doi10.4274/nkmj.galenos.2023.09226
dc.identifier.endpage264en_US
dc.identifier.issn2587-0262
dc.identifier.issue3en_US
dc.identifier.startpage257en_US
dc.identifier.urihttps://doi.org/10.4274/nkmj.galenos.2023.09226
dc.identifier.urihttps://hdl.handle.net/20.500.14551/20330
dc.identifier.volume11en_US
dc.identifier.wosWOS:001187553300013en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.language.isoenen_US
dc.publisherGalenos Publ Houseen_US
dc.relation.ispartofNamik Kemal Medical Journalen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectDactinomycinen_US
dc.subjectGalanginen_US
dc.subjectAML-12 Cell Lineen_US
dc.subjectHepatotoxicityen_US
dc.subjectOxidative Stressen_US
dc.subjectApoptosisen_US
dc.subjectHepatopathy-Thrombocytopenia Syndromeen_US
dc.subjectHepatocellular-Carcinomaen_US
dc.subjectApoptosisen_US
dc.subjectMechanismsen_US
dc.titleGalangin Protects AML-12 Cells Against Dactinomycin Induced Hepatotoxicityen_US
dc.typeArticleen_US

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