Diazoxide attenuates DOX-induced cardiotoxicity in cultured rat myocytes

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dc.authoridSevgiler, Yusuf/0000-0002-4373-2389en_US
dc.authorscopusid6602873428en_US
dc.authorscopusid36543258600en_US
dc.authorscopusid58925924400en_US
dc.authorscopusid55515395600en_US
dc.authorscopusid56152285300en_US
dc.authorwosidSevgiler, Yusuf/S-7015-2016en_US
dc.contributor.authorGuven, Celal
dc.contributor.authorTaskin, Eylem
dc.contributor.authorAydin, Ozgul
dc.contributor.authorKaya, Salih Tunc
dc.contributor.authorSevgiler, Yusuf
dc.date.accessioned2024-08-23T16:04:28Z
dc.date.available2024-08-23T16:04:28Z
dc.date.issued2024en_US
dc.departmentDüzce Üniversitesien_US
dc.description.abstractDoxorubicin (DOX)-induced cardiotoxicity is a well known clinical problem, and many investigations have been made of its possible amelioration. We have investigated whether diazoxide (DIA), an agonist at mitochondrial ATP-sensitive potassium channels (mitoKATP), could reverse DOX-induced apoptotic myocardial cell loss, in cultured rat cardiomyocytes. The role of certain proteins in this pathway was also studied. The rat cardiomyocyte cell line (H9c2) was treated with DOX, and also co-treated with DOX and DIA, for 24 h. Distribution of actin filaments, mitochondrial membrane potential, superoxide dismutase (SOD) activity, total oxidant and antioxidant status (TOS and TAS, respectively), and some protein expressions, were assessed. DOX significantly decreased SOD activity, increased ERK1/2 protein levels, and depolarised the mitochondrial membrane, while DIA co-treatment inhibited such changes. DIA co-treatment ameliorated DOX-induced cytoskeletal changes via F-actin distribution and mitoKATP structure. Co-treatment also decreased ERK1/2 and cytochrome c protein levels. Cardiomyocyte loss due to oxidative stress-mediated apoptosis is a key event in DOX-induced cytotoxicity. DIA had protective effects on DOX-induced cardiotoxicity, via mitoKATP integrity, especially with elevated SUR2A levels; but also by a cascade including SOD/AMPK/ERK1/2. Therefore, DIA may be considered a candidate agent for protecting cardiomyocytes against DOX chemotherapy.en_US
dc.description.sponsorshipAdimath;yaman University Scientific Research Commission [FEFYL/2018-0001]en_US
dc.description.sponsorshipWe gratefully acknowledge Ad & imath;yaman University Scientific Research Commission for their support by provision of Grant no. FEFYL/2018-0001. We also thank Dr Muhsin Ayd & imath;n for editing the manuscript.en_US
dc.identifier.doi10.1080/10520295.2024.2324368
dc.identifier.endpage124en_US
dc.identifier.issn1052-0295
dc.identifier.issn1473-7760
dc.identifier.issue3en_US
dc.identifier.pmid38439686en_US
dc.identifier.scopus2-s2.0-85187187292en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage113en_US
dc.identifier.urihttps://doi.org/10.1080/10520295.2024.2324368
dc.identifier.urihttps://hdl.handle.net/20.500.12684/14210
dc.identifier.volume99en_US
dc.identifier.wosWOS:001179066800001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofBiotechnic & Histochemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApoptosisen_US
dc.subjectATP-sensitive potassium channelsen_US
dc.subjectdiazoxideen_US
dc.subjectdoxorubicinen_US
dc.subjectoxidative stressen_US
dc.subjectSensitive Potassium Channelsen_US
dc.subjectActivated Protein-Kinaseen_US
dc.subjectK-Atp Channelsen_US
dc.subjectActin Cytoskeletonen_US
dc.subjectAngiotensin-Iien_US
dc.subjectCardioprotectionen_US
dc.subjectMitochondriaen_US
dc.subjectDoxorubicinen_US
dc.subjectPhosphorylationen_US
dc.subjectDysfunctionen_US
dc.titleDiazoxide attenuates DOX-induced cardiotoxicity in cultured rat myocytesen_US
dc.typeArticleen_US

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