Abstract

In 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 μl. 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.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call