Parameters of Oxidative Stress and Behavior in Animals Treated with Dexametasone and Submitted to Pentylenetetrazol Kindling.
Dexamethasone
Oxidative stress
Pentylenetetrazole
Journal
Journal of epilepsy research
ISSN: 2233-6249
Titre abrégé: J Epilepsy Res
Pays: Korea (South)
ID NLM: 101577886
Informations de publication
Date de publication:
Dec 2021
Dec 2021
Historique:
received:
27
04
2021
revised:
29
06
2021
accepted:
20
10
2021
entrez:
28
1
2022
pubmed:
29
1
2022
medline:
29
1
2022
Statut:
epublish
Résumé
Oxidative stress (OS) is defined as an excessive production of reactive oxygen species that cannot be neutralized by the action of antioxidants, but also as an alteration of the cellular redox balance. The relationship between OS and epilepsy is not yet fully understood. The objective of this study was to evaluate the effect of dexamethasone on OS levels and memory in the kindling model induced by pentylenetetrazole. The animals were divided in six groups: control group that received no treatment, vehicle group treated with vehicle, diazepam group, and groups treated with dexamethasone (1, 2 and 4 mg/kg). Treated animals received pentylenetetrazole in alternated days for 15 days. Inhibitory avoidance test was conducted in 2 hours and OS was evaluated after animal sacrifice. Regarding the treatment with dexamethasone, there was no significant difference when compared to the control groups in relation to the inhibitory avoidance test. On OS levels, there was a decrease in catalase activity levels in the hippocampus and an increase in thiobarbituric acid reactive substances and glutathione peroxidase levels in the hippocampus. The anticonvulsant effect of dexametasone remains uncertain. Immunological mechanisms, with the release of cytokines and inflammatory mediators, seem to be the key to this process. The mechanisms that generate OS are probably related to the anticonvulsant effects found.
Sections du résumé
BACKGROUND AND PURPOSE
OBJECTIVE
Oxidative stress (OS) is defined as an excessive production of reactive oxygen species that cannot be neutralized by the action of antioxidants, but also as an alteration of the cellular redox balance. The relationship between OS and epilepsy is not yet fully understood. The objective of this study was to evaluate the effect of dexamethasone on OS levels and memory in the kindling model induced by pentylenetetrazole.
METHODS
METHODS
The animals were divided in six groups: control group that received no treatment, vehicle group treated with vehicle, diazepam group, and groups treated with dexamethasone (1, 2 and 4 mg/kg). Treated animals received pentylenetetrazole in alternated days for 15 days. Inhibitory avoidance test was conducted in 2 hours and OS was evaluated after animal sacrifice.
RESULTS
RESULTS
Regarding the treatment with dexamethasone, there was no significant difference when compared to the control groups in relation to the inhibitory avoidance test. On OS levels, there was a decrease in catalase activity levels in the hippocampus and an increase in thiobarbituric acid reactive substances and glutathione peroxidase levels in the hippocampus.
CONCLUSIONS
CONCLUSIONS
The anticonvulsant effect of dexametasone remains uncertain. Immunological mechanisms, with the release of cytokines and inflammatory mediators, seem to be the key to this process. The mechanisms that generate OS are probably related to the anticonvulsant effects found.
Identifiants
pubmed: 35087719
doi: 10.14581/jer.21017
pii: jer-21017
pmc: PMC8767226
doi:
Types de publication
Journal Article
Langues
eng
Pagination
113-119Informations de copyright
Copyright © 2021 Korean Epilepsy Society.
Déclaration de conflit d'intérêts
Conflict of Interest The authors declare that they have no conflicts of interest.
Références
Int J Med Sci. 2020 Jul 2;17(12):1683-1691
pubmed: 32714071
Neurobiol Learn Mem. 2007 Sep;88(2):160-6
pubmed: 17562373
Annu Rev Biochem. 2017 Jun 20;86:715-748
pubmed: 28441057
Neurosci Lett. 2001 Apr 20;302(2-3):141-5
pubmed: 11290407
Hippocampus. 2014 May;24(5):510-5
pubmed: 24596244
Food Chem. 2019 Jan 1;270:25-31
pubmed: 30174042
Can J Physiol Pharmacol. 2019 Jan;97(1):37-46
pubmed: 30308130
Oxid Med Cell Longev. 2016;2016:5698931
pubmed: 26881031
Neurochem Int. 2012 Jun;60(8):799-805
pubmed: 22465942
Epilepsia Open. 2018 Jul 16;3(Suppl Suppl 2):133-142
pubmed: 30564772
Methods Enzymol. 1984;105:121-6
pubmed: 6727660
Antioxid Redox Signal. 2013 Apr 20;18(12):1475-90
pubmed: 22746161
Eur J Med Chem. 2015 Jun 5;97:55-74
pubmed: 25942353
J Neuroimmunol. 2018 Dec 15;325:92-98
pubmed: 30316679
3 Biotech. 2018 Aug;8(8):363
pubmed: 30105188
Expert Rev Neurother. 2018 May;18(5):427-434
pubmed: 29651881
Curr Clin Pharmacol. 2019;14(1):68-75
pubmed: 30465512
Methods Biochem Anal. 1987;32:279-312
pubmed: 3033431
Curr Neuropharmacol. 2009 Mar;7(1):65-74
pubmed: 19721819
Anat Cell Biol. 2020 Mar;53(1):84-94
pubmed: 32274253
Brain Res Bull. 2013 Mar;92:60-8
pubmed: 23270878