FOLFIRI-Mediated Toxicity in Human Aortic Smooth Muscle Cells and Possible Amelioration with Curcumin and Quercetin

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dc.authoridDoganlar, Zeynep Banu/0000-0002-1365-9897
dc.authoridDoganlar, Oguzhan/0000-0003-2654-7269
dc.authoridYuksel, Volkan/0000-0001-9518-2588
dc.authoridGUCLU, Orkut/0000-0001-6460-3175
dc.authorwosidDoğanlar, Oğuzhan/A-2315-2019
dc.authorwosidDoganlar, Zeynep Banu/B-4845-2008
dc.authorwosidGUCLU, Orkut/H-9993-2014
dc.contributor.authorGuclu, Orkut
dc.contributor.authorDoganlar, Oguzhan
dc.contributor.authorYuksel, Volkan
dc.contributor.authorDoganlar, Zeynep Banu
dc.date.accessioned2024-06-12T11:02:04Z
dc.date.available2024-06-12T11:02:04Z
dc.date.issued2020
dc.departmentTrakya Üniversitesien_US
dc.description.abstractSystemic chemotherapy-mediated cell toxicity is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events of the FOLFIRI (irinotecan, folinic acid and 5-fluorouracil) regimen are mainly due to DNA damage induced by antimetabolite and topoisomerase inhibition effects. However, the role of human aortic smooth muscle cells (HaVSMCs) in this process and the mechanisms of oxidative stress, DNA and protein damage and apoptosis have not been investigated. Therefore, the effects of curcumin and quercetin on HaVSMC survival in the generation of molecular and cellular toxicity by FOLFIRI treatment and the involvement of vital cellular signalling pathways were investigated. We analysed both FOLFIRI toxicity and the therapeutic potential of quercetin and curcumin in terms of HaVSMC damage using molecular probe and florescence staining, Random Amplified Polymorphic DNA (RAPD), qRT-PCR and Western blot assays. Our study presents two preliminary findings: (a) in HaVSMCs, FOLFIRI treatment significantly induces oxidative damage to both DNA and protein, leading to a dramatic increase in caspase-dependent apoptotic death through P53-mediated Caspase3-dependent mitochondrial apoptosis, and results in TNF-alpha/Caspase8-mediated necrotic death, and (b) flavonoids not only regulate the expression of genes encoding antioxidant enzymes and increase DNA damage but also limit programmed and necrotic cell death processes in HaVSMCs. Our results clearly indicate the potential for curcumin and, particularly, quercetin as preventative chemotherapeutic interventions for cardiovascular toxicity induced by the FOLFIRI regime in HaVSMCs.en_US
dc.identifier.doi10.1007/s12012-019-09541-w
dc.identifier.endpage154en_US
dc.identifier.issn1530-7905
dc.identifier.issn1559-0259
dc.identifier.issue2en_US
dc.identifier.pmid31278615en_US
dc.identifier.scopus2-s2.0-85068819649en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage139en_US
dc.identifier.urihttps://doi.org/10.1007/s12012-019-09541-w
dc.identifier.urihttps://hdl.handle.net/20.500.14551/21138
dc.identifier.volume20en_US
dc.identifier.wosWOS:000519667100005en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherHumana Press Incen_US
dc.relation.ispartofCardiovascular Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectFOLFIRIen_US
dc.subjectCardiotoxicityen_US
dc.subjectGenotoxicityen_US
dc.subjectOxidative Stressen_US
dc.subjectHuman Aortic Smooth Muscle Cellsen_US
dc.subjectMetastatic Colorectal-Canceren_US
dc.subjectInduced Dna-Damageen_US
dc.subjectHydrogen-Peroxideen_US
dc.subjectOxidative Stressen_US
dc.subject2nd-Line Chemotherapyen_US
dc.subjectInduced Apoptosisen_US
dc.subjectIrinotecanen_US
dc.subjectInhibitionen_US
dc.subjectFlavonoidsen_US
dc.subjectTherapyen_US
dc.titleFOLFIRI-Mediated Toxicity in Human Aortic Smooth Muscle Cells and Possible Amelioration with Curcumin and Quercetinen_US
dc.typeArticleen_US

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