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Titolo:
Effects of COX-2 inhibitors on aortic prostacyclin production in cholesterol-fed rabbits
Autore:
Wong, E; Huang, JQ; Tagari, P; Riendeau, D;
Indirizzi:
Merck Frosst Ctr Therapeut Res, Dept Biochem & Mol Biol, Kirkland, PQ H9H 3L1, Canada Merck Frosst Ctr Therapeut Res Kirkland PQ Canada H9H 3L1 H9H 3L1, Canada Merck Frosst Ctr Therapeut Res, Dept Pharmacol, Kirkland, PQ H9H 3L1, Canada Merck Frosst Ctr Therapeut Res Kirkland PQ Canada H9H 3L1 H9H 3L1, Canada
Titolo Testata:
ATHEROSCLEROSIS
fascicolo: 2, volume: 157, anno: 2001,
pagine: 393 - 402
SICI:
0021-9150(200108)157:2<393:EOCIOA>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; SMOOTH-MUSCLE CELLS; CYCLOOXYGENASE-1 GENE-EXPRESSION; PULMONARY-ARTERY ENDOTHELIUM; PROSTAGLANDIN G/H SYNTHASE-1; FAT-FED RABBITS; ATHEROSCLEROTIC LESIONS; CORONARY-ARTERIES; UP-REGULATION; SHEAR-STRESS;
Keywords:
atherosclerosis; cyclooxygenase; NSAID; prostacyclin; prostaglandin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Riendeau, D Merck Frosst Ctr Therapeut Res, Dept Biochem & Mol Biol, 16711Trans Canada Hwy, Kirkland, PQ H9H 3L1, Canada Merck Frosst Ctr Therapeut Res 16711 Trans Canada Hwy Kirkland PQ Canada H9H 3L1
Citazione:
E. Wong et al., "Effects of COX-2 inhibitors on aortic prostacyclin production in cholesterol-fed rabbits", ATHEROSCLER, 157(2), 2001, pp. 393-402

Abstract

Prostacyclin (PGI(2)) is a potent vasodilator and inhibitor of platelet aggregation that is produced by prostacyclin synthase via the cyclooxygenase (COX) pathway of arachidonic acid metabolism. We investigated the potentialrole of COX-2 in the production of vasoactive prostanoids by aortic tissuein a rabbit model of dietary cholesterol-induced atherosclerosis. COX-1 was detected as the major isoform by immunoblot analysis in extracts from aortas of normal and 8 week cholesterol-fed animals with COX-2 being induced in atherosclerotic plaques from cholesterol-fed animals. Aortic tissue from cholesterol-fed animals showed decreased levels of basal 6-keto-PGF(1 alpha) and PGE(2) production as compared to the normal controls but showed no difference with respect to their ability to synthesize these prostanoids in response to exogenous arachidonic acid. The highly selective COX-2 inhibitors rofecoxib and the furanone DFP at concentrations of up to 10 mu mol/l hadno effect on the arachidonic acid-dependent production of 6-keto-PGF(1 alpha), in contrast to indomethacin, which caused a complete inhibition at 0.5mu mol/l. Celecoxib caused a significant inhibition of 6-keto-PGF(1 alpha)at 10 mu mol/l but had little effect when the dose was lowered to 1 mu mol/l. Similar effects of these inhibitors were observed with respect to the production of PGE, and no major difference was observed between aortic tissues from normal and cholesterol-fed animals with regard to inhibitor sensitivity. These results indicate that in a rabbit model of early stage cardiovascular disease, the basal production of 6-keto-PGF1 alpha and PGE(2) by aortic tissue is decreased. Furthermore, COX-2 expression is induced in atherosclerotic plaques and may play a role in altering localized synthesis of prostanoids in these lesions but does not appear to significantly impact the arachidonic acid-dependent prostacylin production of aortic tissues, which is largely mediated by COX-1. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 18:54:31