Dexketoprofene, selective cox-1 inhibitor nsaids, without gastrointestinal injury in rats

Dexketoprofene, selective cox-1 inhibitor nsaids, without gastrointestinal injury in rats

Dexketoprofene (De) NSAID was studied as a selective COX-1 inhibitor in comparison with Ketorolac (Ke), a mainly COX-1 inhibitor. De and Ke were administered to different groups of animals in a dose-dependent manner, i.e., 3-15 and 25 mgs/kg. The gastrointestinal mucosa damage was macroscopically an...

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Bibliographic Details
Published in:Acta gastroenterologica latinoamericana Vol. 32; no. 1; p. 17
Main Authors: Laudanno, O M, Piombo, Gabriela, Cesolari, J A M, Godoy, Alicia, Rocaspana, Adriana, Aramberry, L
Format: Journal Article
Language:Spanish
Published: Argentina 01-05-2002
Subjects:
Analysis of Variance
Animals
Anti-Inflammatory Agents, Non-Steroidal - adverse effects
Celecoxib
Cyclooxygenase Inhibitors - adverse effects
Drug Evaluation, Preclinical
Gastric Mucosa - drug effects
Humans
Intestinal Mucosa - drug effects
Ketoprofen - adverse effects
Ketoprofen - analogs & derivatives
Ketorolac - pharmacology
Pyrazoles
Rats
Rats, Wistar
Sulfonamides - pharmacology
Tromethamine - adverse effects
Tromethamine - analogs & derivatives
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Summary:Dexketoprofene (De) NSAID was studied as a selective COX-1 inhibitor in comparison with Ketorolac (Ke), a mainly COX-1 inhibitor. De and Ke were administered to different groups of animals in a dose-dependent manner, i.e., 3-15 and 25 mgs/kg. The gastrointestinal mucosa damage was macroscopically and microscopically quantified at 24 hs, as well as leukocyte infiltration (LI) and neosinophilia. Similarly, Indomethacin (Indo) damage (COX-1-COX-2), with 25 mgs/kg. Dose was compared. On the other hand, De and Ke at inhibitory selective COX-1 dose (3 mg/kg) plus Celecoxib, selective COX-2 inhibitor, yielding no gastrointestinal damage, with decreased LI and without neutrophilia, the same as Ke (n.s.). Similarly De at higher dose (2.5 mgs/kg), produced minimal gastrointestinal lesions, showing a preferential COX-1 inhibitor behavior. Ke and Indo produced important gastrointestinal necrotic and erosive lesions with remarkable LI and neutrophilia (p < 0.001). On the other hand, COX-1 De dose plus Celecoxib produced evident gastrointestinal lesions, increased LI and neutrophilia, the same as Indo, pointing out that the gastrointestinal damage is due to COX-1 and COX-2 inhibition.
ISSN:0300-9033