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Titolo:
Effects of meloxicam on oxygen radical generation in rat gastric mucosa
Autore:
Villegas, I; Martin, MJ; La Casa, C; Motilva, V; de la Lastra, CA;
Indirizzi:
Univ Sevilla, Fac Pharm, Dept Pharmacol, E-41012 Seville, Spain Univ Sevilla Seville Spain E-41012 ept Pharmacol, E-41012 Seville, Spain
Titolo Testata:
INFLAMMATION RESEARCH
fascicolo: 7, volume: 49, anno: 2000,
pagine: 361 - 366
SICI:
1023-3830(200007)49:7<361:EOMOOR>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ARACHIDONIC-ACID METABOLISM; LIPID-PEROXIDATION; INJURY; INDOMETHACIN; GLUTATHIONE; EXPRESSION; MECHANISMS; ASPIRIN;
Keywords:
non-steroidal anti-inflammatory drugs (NSAIDs) meloxicam; COX-2 inhibitors; gastric injury; oxygen radical;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: de la Lastra, CA Univ Sevilla, Fac Pharm, Dept Pharmacol, C Prof Garcia Gonzalez, E-41012 Seville, Spain Univ Sevilla C Prof Garcia Gonzalez SevilleSpain E-41012
Citazione:
I. Villegas et al., "Effects of meloxicam on oxygen radical generation in rat gastric mucosa", INFLAMM RES, 49(7), 2000, pp. 361-366

Abstract

Aim and Design. In addition to a deficiency of endogenous prostaglandins due to inhibition of cyclo-oxygenase and a host of prostaglandin-mediated effects on mucosal protection, it has recently been proposed that neutrophil-oxygen radical - dependent microvascular injuries may be important prime events that lead to mucosal injury induced by non-steroidal anti-inflammatory drugs. Therefore, we evaluated the role of oxygen free radicals in the pathogenesis of acute gastric ulceration induced by meloxicam, a preferentialCOX-2 inhibitor. Material: Studies were performed in Wistar rats. Treatment: Meloxicam was given by oral administration (3.75-30 mg/kg body weight). Methods: Determinations were made of gastric mucosal injury, xanthine-oxidase, myeloperoxidase and superoxide dismutase activities, as well as the effect of meloxicam on gastric prostaglandin synthesis (PGE, levels) and glutathione homeostasis. Results: Oral administration of meloxicam dose-dependently (3.75-30 mg/kg)caused acute gastric haemorrhage erosions. The total area of gastric lesions increased with time until 24 hours after dosing. Xanthine-oxidase activity increased significantly after administration of the drug. Myeloperoxidase activity, as an index of neutrophil infiltration, as well as glutathione peroxidase, an important enzyme that scavenges lipid peroxides, were unaffected by meloxicam administration. In addition, superoxide dismutase activity, PGE(2) and glutathione levels were significantly reduced. Conclusion. These results support the hypothesis that in addition to suppresion of prostaglandin synthesis, oxygen free radicals, probably derived via the action of xanthine oxidase, the decrease in superoxide dismutase activity, and the depletion of mucosal glutathione contribute to the pathogenesis of meloxicam-induced ulceration.

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Documento generato il 03/04/20 alle ore 08:04:55