COX-2 Inhibition by Diclofenac Is Associated With Decreased Apoptosis and Lesion Area After Experimental Focal Penetrating Traumatic Brain Injury in Rats.
NSAID
cyklooxygenase-2
diclofenac
focal penetrating TBI
traumatic brain injury
Journal
Frontiers in neurology
ISSN: 1664-2295
Titre abrégé: Front Neurol
Pays: Switzerland
ID NLM: 101546899
Informations de publication
Date de publication:
2019
2019
Historique:
received:
23
09
2018
accepted:
15
07
2019
entrez:
17
8
2019
pubmed:
17
8
2019
medline:
17
8
2019
Statut:
epublish
Résumé
Traumatic brain injury (TBI) is followed by a secondary inflammation in the brain. The inflammatory response includes prostanoid synthesis by the inducible enzyme cyclooxygenase-2 (COX-2). Inhibition of COX-2 is associated with improved functional outcome in experimental TBI models, although central nervous system-specific effects are not fully understood. Animal studies report better outcomes in females than males. The exact mechanisms for this gender dichotomy remain unknown. In an initial study we reported increased COX-2 expression in male rats, compared to female, following experimental TBI. It is possible that COX-2 induction is directly associated with increased cell death after TBI. Therefore, we designed a sequential study to investigate the blocking of COX-2 specifically, using the established COX-2 inhibitor diclofenac. Male Sprague-Dawley rats weighing between 250 and 350 g were exposed to focal penetrating TBI and randomly selected for diclofenac treatment (5 μg intralesionally, immediately following TBI) (
Identifiants
pubmed: 31417487
doi: 10.3389/fneur.2019.00811
pmc: PMC6682700
doi:
Types de publication
Journal Article
Langues
eng
Pagination
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