The effects of ATP sensitive potassium channel (KATP) opener and blockers on Bcl-2, Bax, and Cyt-c gene expression levels in epileptic rats

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dc.authorscopusid57194432176
dc.authorscopusid57219390008
dc.contributor.authorKiliç, Ümit
dc.contributor.authorSoytürk, Hayriye
dc.date.accessioned2024-09-25T19:44:12Z
dc.date.available2024-09-25T19:44:12Z
dc.date.issued2022
dc.departmentAbant İzzet Baysal Üniversitesien_US
dc.description.abstractIn this study, it was aimed to investigate the gene expression levels of Bcl-2, Bax, and cytochrome c (Cyt-c), in the cortex region of pinacidil as a KATP channel opener and glibenclamide as a blocker on penicillin model epilepsy. Male Wistar-Albino rats were used. A total of 4 main groups were formed: Control, Epilepsy, Epilepsy-opener, and Epilepsy-blocker groups, then three-time points were formed subgroups (1st day, 4th, and 8th). 48 rats were used in total. The epileptic focus was created by intracortical administration of penicillin at a dose of 500 IU/2 ?l. Cortex is removed from all animals and cyt c, Bcl-2, and Bax gene expression levels were determined by qPCR. The SPSS 21 program was used for statistics. Bcl-2 and Bax gene expression levels were increased in the cortex regions of rats with epilepsy (p<0.05). Bcl-2, Bax gene expression levels, which increased due to epilepsy with the effect of KATP channels opened with pinacidil, returned to normal levels in the epilepsy opener group (p<0.05). Bcl-2 gene expression level, which was increased as a result of epilepsy due to the effect of KATP channels closed with glibenclamide, was higher than in the control and epilepsy-opener groups (p<0.05). Bcl-2 and Bax gene expression levels are increased in the cortex region due to epilepsy indicates that the apoptotic pathway could be activated. This study also It has been shown that the apoptotic pathway activated by epilepsy can be inactivated by pinacidil. © 2022 Ondokuz Mayis Universitesi. All rights reserved.en_US
dc.description.sponsorshipAbant İzzet Baysal University Research Foundation, (2019.10.01.1408)en_US
dc.identifier.doi10.52142/omujecm.39.3.50
dc.identifier.endpage862en_US
dc.identifier.issn1309-4483
dc.identifier.issue3en_US
dc.identifier.scopus2-s2.0-85142102884en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage857en_US
dc.identifier.urihttps://doi.org/10.52142/omujecm.39.3.50
dc.identifier.urihttps://hdl.handle.net/20.500.12491/12715
dc.identifier.volume39en_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherOndokuz Mayis Universitesien_US
dc.relation.ispartofJournal of Experimental and Clinical Medicine (Turkey)en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmzYK_20240925en_US
dc.subjectBaxen_US
dc.subjectBcl-2en_US
dc.subjectCytochrome cen_US
dc.subjectepilepsyen_US
dc.subjectKATP channelsen_US
dc.titleThe effects of ATP sensitive potassium channel (KATP) opener and blockers on Bcl-2, Bax, and Cyt-c gene expression levels in epileptic ratsen_US
dc.typeArticleen_US

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