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Relation between Proepileptic Activity of Indomethacin and AdrenalGland Hormones

The role of inflammation has been shown in the pathogenesis of epilepsy, while glucocorticoids and adrenaline have anti-inflammatory effects. The aim of the present study was to investigate the effects of adrenaline, prednisolone, and indomethacin on caffeine-induced epilepsy (epileptiform activity)...

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Autores principales: Hacimuftuoglu, Ahmet, Suleyman, Halis, Cadirci, Elif, Albayrak, Abdulmecit, Polat, Beyzagul, Hakan Alp, Hamit, Halici, Zekai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Shaheed Beheshti University of Medical Sciences 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3813114/
https://www.ncbi.nlm.nih.gov/pubmed/24250522
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author Hacimuftuoglu, Ahmet
Suleyman, Halis
Cadirci, Elif
Albayrak, Abdulmecit
Polat, Beyzagul
Hakan Alp, Hamit
Halici, Zekai
author_facet Hacimuftuoglu, Ahmet
Suleyman, Halis
Cadirci, Elif
Albayrak, Abdulmecit
Polat, Beyzagul
Hakan Alp, Hamit
Halici, Zekai
author_sort Hacimuftuoglu, Ahmet
collection PubMed
description The role of inflammation has been shown in the pathogenesis of epilepsy, while glucocorticoids and adrenaline have anti-inflammatory effects. The aim of the present study was to investigate the effects of adrenaline, prednisolone, and indomethacin on caffeine-induced epilepsy (epileptiform activity) in rats and to examine the mechanism of the pro-epileptic effect of indomethacin. The adrenalectomized rats that had been given only adrenaline (the control group) did not die; however, adrenaline did not prevent the adrenalectomized rats which were given prazosin, phenoxybenzamine, yohimbine, metoprolol, and propranolol from dying. In the rats given propranolol + adrenaline, the rate of death was 100%, while this rate was 50% in the groups receiving prazosin + adrenaline, phenoxybenzamine + adrenaline, and metoprolol + adrenaline. The rate was 75% in the group given yohimbine + adrenaline. Prednisolone increased the degree of convulsion in adrenalectomized rats. Over-reduction in the blood catecholamine level made epileptogenesis more severe. It was observed that adrenaline pressed epileptogenesis via its own receptors (α - 1, α - 2, β - 1, β - 2). It was also revealed that all of the adrenergic receptors were responsible due to antiepileptic activity; β - 2 receptors played the most important role. It was observed that both acute and chronic indomethacin administration reduced the catecholamine levels. The situation in which acute administration of indomethacin did not affect epileptogenesis might originate from the fact that the structure of indomethacin did not significantly increase the corticosterone level.
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spelling pubmed-38131142013-11-18 Relation between Proepileptic Activity of Indomethacin and AdrenalGland Hormones Hacimuftuoglu, Ahmet Suleyman, Halis Cadirci, Elif Albayrak, Abdulmecit Polat, Beyzagul Hakan Alp, Hamit Halici, Zekai Iran J Pharm Res Original Article The role of inflammation has been shown in the pathogenesis of epilepsy, while glucocorticoids and adrenaline have anti-inflammatory effects. The aim of the present study was to investigate the effects of adrenaline, prednisolone, and indomethacin on caffeine-induced epilepsy (epileptiform activity) in rats and to examine the mechanism of the pro-epileptic effect of indomethacin. The adrenalectomized rats that had been given only adrenaline (the control group) did not die; however, adrenaline did not prevent the adrenalectomized rats which were given prazosin, phenoxybenzamine, yohimbine, metoprolol, and propranolol from dying. In the rats given propranolol + adrenaline, the rate of death was 100%, while this rate was 50% in the groups receiving prazosin + adrenaline, phenoxybenzamine + adrenaline, and metoprolol + adrenaline. The rate was 75% in the group given yohimbine + adrenaline. Prednisolone increased the degree of convulsion in adrenalectomized rats. Over-reduction in the blood catecholamine level made epileptogenesis more severe. It was observed that adrenaline pressed epileptogenesis via its own receptors (α - 1, α - 2, β - 1, β - 2). It was also revealed that all of the adrenergic receptors were responsible due to antiepileptic activity; β - 2 receptors played the most important role. It was observed that both acute and chronic indomethacin administration reduced the catecholamine levels. The situation in which acute administration of indomethacin did not affect epileptogenesis might originate from the fact that the structure of indomethacin did not significantly increase the corticosterone level. Shaheed Beheshti University of Medical Sciences 2012 /pmc/articles/PMC3813114/ /pubmed/24250522 Text en © 2012 by School of Pharmacy, Shaheed Beheshti University of Medical Sciences and Health Services This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Hacimuftuoglu, Ahmet
Suleyman, Halis
Cadirci, Elif
Albayrak, Abdulmecit
Polat, Beyzagul
Hakan Alp, Hamit
Halici, Zekai
Relation between Proepileptic Activity of Indomethacin and AdrenalGland Hormones
title Relation between Proepileptic Activity of Indomethacin and AdrenalGland Hormones
title_full Relation between Proepileptic Activity of Indomethacin and AdrenalGland Hormones
title_fullStr Relation between Proepileptic Activity of Indomethacin and AdrenalGland Hormones
title_full_unstemmed Relation between Proepileptic Activity of Indomethacin and AdrenalGland Hormones
title_short Relation between Proepileptic Activity of Indomethacin and AdrenalGland Hormones
title_sort relation between proepileptic activity of indomethacin and adrenalgland hormones
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3813114/
https://www.ncbi.nlm.nih.gov/pubmed/24250522
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