Effect of the selective mitochondrial KATP channel opener nicorandil on the QT prolongation and myocardial damage induced by amitriptyline in rats
dc.authorid | AKAN, PINAR/0000-0001-9211-1944 | |
dc.authorid | Akturk, Gozde/0000-0003-1343-4361 | |
dc.authorid | HOCAOGLU AKSAY, NIL/0000-0002-7449-6809 | |
dc.authorid | Kalkan, Sule/0000-0002-0364-7390 | |
dc.authorid | GURSOY CALAN, OZLEM/0000-0002-1312-3777 | |
dc.authorid | ergur, bekir/0000-0002-6448-2593 | |
dc.authorid | Sahin, Orhan/0000-0003-1606-3164 | |
dc.contributor.author | Sahin, Orhan | |
dc.contributor.author | Akturk, Gozde | |
dc.contributor.author | Micili, Serap Cilaker | |
dc.contributor.author | Doruk, Ozlem Gursoy | |
dc.contributor.author | Karapinar, Fazilet | |
dc.contributor.author | Hocaoglu, Nil | |
dc.contributor.author | Ergur, Bekir Ugur | |
dc.date.accessioned | 2024-09-18T19:54:16Z | |
dc.date.available | 2024-09-18T19:54:16Z | |
dc.date.issued | 2023 | |
dc.department | Hatay Mustafa Kemal Üniversitesi | en_US |
dc.description.abstract | Objectives The aim of this study is to evaluate the protective effect of nicorandil, a selective mitochondrial K-ATP channel opener, on QT prolongation and myocardial damage induced by amitriptyline. Methods The dose of amitriptyline (intraperitoneal, i.p.) that prolong the QT interval was found 75 mg/kg. Rats were randomized into five groups the control group, amitriptyline group, nicorandil (selective mitochondrial K-ATP channel opener, 3 mg/kg i.p.) + amitriptyline group, 5-hdyroxydecanoate (5-HD, selective mitochondrial K-ATP channel blocker, 10 mg/kg i.p.) + amitriptyline group and 5-HD + nicorandil + amitriptyline group. Cardiac parameters, biochemical and histomorphological/immunohistochemical examinations were evaluated. p < 0.05 was accepted as statistically significant. Key findings Amitriptyline caused statistically significant prolongation of QRS duration, QT interval and QTc interval (p < 0.05). It also caused changes in tissue oxidant (increase in malondialdehyde)/anti-oxidant (decrease in glutathione peroxidase) parameters (p < 0.05), myocardial damage and apoptosis (p < 0.01 and p < 0.001). While nicorandil administration prevented amitriptyline-induced QRS, QT, QTc prolongation (p < 0.05), myocardial damage and apoptosis (p < 0.05), it did not affect the changes in oxidative parameters (p > 0.05). Conclusions Our results suggest that nicorandil, a selective mitochondrial K-ATP channel opener, plays a protective role in amitriptyline-induced QT prolongation and myocardial damage. Mitochondrial K-ATP channel opening and anti-apoptotic effects may play a role in the cardioprotective effect of nicorandil. | en_US |
dc.identifier.doi | 10.1093/jpp/rgac089 | |
dc.identifier.endpage | 426 | en_US |
dc.identifier.issn | 0022-3573 | |
dc.identifier.issn | 2042-7158 | |
dc.identifier.issue | 3 | en_US |
dc.identifier.pmid | 36527252 | en_US |
dc.identifier.scopus | 2-s2.0-85150079473 | en_US |
dc.identifier.scopusquality | Q2 | en_US |
dc.identifier.startpage | 415 | en_US |
dc.identifier.uri | https://doi.org/10.1093/jpp/rgac089 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12483/7615 | |
dc.identifier.volume | 75 | en_US |
dc.identifier.wos | WOS:000898595600001 | en_US |
dc.identifier.wosquality | Q2 | en_US |
dc.indekslendigikaynak | Web of Science | en_US |
dc.indekslendigikaynak | Scopus | en_US |
dc.indekslendigikaynak | PubMed | en_US |
dc.language.iso | en | en_US |
dc.publisher | Oxford Univ Press | en_US |
dc.relation.ispartof | Journal of Pharmacy and Pharmacology | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | amitriptyline | en_US |
dc.subject | nicorandil | en_US |
dc.subject | QT prolongation | en_US |
dc.subject | cardiotoxicity | en_US |
dc.subject | mitoK(ATP) channel | en_US |
dc.title | Effect of the selective mitochondrial KATP channel opener nicorandil on the QT prolongation and myocardial damage induced by amitriptyline in rats | en_US |
dc.type | Article | en_US |
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