A novel sulindac derivative protects against oxidative damage by a cyclooxygenase-independent mechanism.
COX-1
COX-2
Oxidative stress
aging
cardiac ischemia
ischemia / reperfusion injury
oxidative injury
oxygen radicals
Journal
The Journal of pharmacology and experimental therapeutics
ISSN: 1521-0103
Titre abrégé: J Pharmacol Exp Ther
Pays: United States
ID NLM: 0376362
Informations de publication
Date de publication:
09 Jun 2022
09 Jun 2022
Historique:
accepted:
03
05
2022
received:
04
01
2022
revised:
30
04
2022
entrez:
9
6
2022
pubmed:
10
6
2022
medline:
10
6
2022
Statut:
aheadofprint
Résumé
Oxidative damage is believed to play a major role in the etiology of many age-related diseases and the normal aging process. We previously reported that sulindac, a cyclooxygenase (COX) inhibitor and FDA approved anti-inflammatory drug, has chemoprotective activity in cells and intact organs by initiating a pharmacological preconditioning response, similar to ischemic preconditioning (IPC). The mechanism is independent of its COX inhibitory activity as suggested by studies on the protection of the heart against oxidative damage from ischemia/reperfusion and retinal pigmented endothelial (RPE) cells against chemical oxidative and UV damage
Identifiants
pubmed: 35680377
pii: jpet.122.001086
doi: 10.1124/jpet.122.001086
pmc: PMC9341458
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIA NIH HHS
ID : P30 AG050911
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA131378
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA155638
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA197147
Pays : United States
Informations de copyright
Copyright © 2020 American Society for Pharmacology and Experimental Therapeutics.
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