Effects of nicorandil on QT prolongation and myocardial damage caused by citalopram in rats

Basit Öğe Kaydı
dc.authoridHOCAOGLU AKSAY, NIL/0000-0002-7449-6809
dc.contributor.authorAkturk, Gozde
dc.contributor.authorMicili, Serap Cilaker
dc.contributor.authorDoruk, Ozlem Gursoy
dc.contributor.authorHocaoglu, Nil
dc.contributor.authorAkan, Pinar
dc.contributor.authorErgur, Bekir Ugur
dc.contributor.authorAhmed, Samar
dc.date.accessioned2024-09-18T20:06:32Z
dc.date.available2024-09-18T20:06:32Z
dc.date.issued2023
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractCitalopram is a selective serotonin re-uptake inhibitor (SSRI) antidepressant; it exhibits the greatest cardiotoxic effect among SSRIs. Citalopram can cause drug-induced long QT syndrome (LQTS) and ventricular arrhythmias. We investigated the protective effect of nicorandil, a selective mitochondrial K-ATP (mito-K-ATP) channel opener, on LQTS and myocardial damage caused by citalopram in male rats. In a preliminary study, we determined that the minimum citalopram dose that prolonged the QT interval was 102 mg/kg injected intraperitoneally. For the main study, rats were divided randomly into five experimental groups: untreated control, normal saline + citalopram, nicorandil + citalopram, 5-hydroxydecanoate (5-HD) + citalopram, 5-HD + nicorandil + citalopram. Biochemical and histologic data from blood and heart tissue samples from six untreated control rats were evaluated. Electrocardiographic parameters including QRS duration, QT interval, corrected QT interval (QTc) and heart rate (HR) were assessed, and biochemical parameters including malondialdehyde, reduced glutathione, glutathione peroxidase, superoxide dismutase were measured. We also performed histomorphologic and immunohistochemical examination of heart tissue. Citalopram prolonged QT-QTc intervals significantly and increased significantly the histomorphologic score and proportion of apoptotic cells, but produced no differences in the oxidant and antioxidant parameters. Nicorandil did not prevent citalopram induced QT-QTc interval prolongation and produced no significant changes in oxidant and antioxidant parameters; however, it did reduce histologic damage and apoptosis caused by citalopram.en_US
dc.description.sponsorshipDokuz Eylul University Scientific Research Projects Coordination Unit [2019, KB.SAG.004]en_US
dc.description.sponsorshipOur work was supported by the Dokuz Eylul University Scientific Research Projects Coordination Unit [Grant no. 2019.KB.SAG.004].en_US
dc.identifier.doi10.1080/10520295.2023.2233417
dc.identifier.endpage491en_US
dc.identifier.issn1052-0295
dc.identifier.issn1473-7760
dc.identifier.issue7en_US
dc.identifier.pmid37466068en_US
dc.identifier.scopus2-s2.0-85165450031en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage479en_US
dc.identifier.urihttps://doi.org/10.1080/10520295.2023.2233417
dc.identifier.urihttps://hdl.handle.net/20.500.12483/8567
dc.identifier.volume98en_US
dc.identifier.wosWOS:001029401000001en_US
dc.identifier.wosqualityQ4en_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.subjectCardiotoxicityen_US
dc.subjectcitalopramen_US
dc.subjectK-ATP channelen_US
dc.subjectlong QT syndromeen_US
dc.subjectnicorandilen_US
dc.subjectratsen_US
dc.titleEffects of nicorandil on QT prolongation and myocardial damage caused by citalopram in ratsen_US
dc.typeArticleen_US

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
[ N/A ]
İsim:
Tam Metin / Full text
Boyut:
1.1 MB
Biçim:
Adobe Portable Document Format
İndir

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayınlar Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu