Meloxicam: influence on arachidonic acid metabolism. Part II. In vivo findings.
作者： G. Engelhardt , R. Bögel , Chr. Schnitzler , R. Utzmann
DOI: 10.1016/0006-2952(95)02110-8
关键词: Diclofenac 、 Tenoxicam 、 Flurbiprofen 、 Endocrinology 、 Piroxicam 、 Cyclooxygenase 、 Tenidap 、 Internal medicine 、 Meloxicam 、 Pharmacology 、 Chemistry 、 In vivo
摘要: Meloxicam is a new nonsteroidal anti-inflammatory drug (NSAID) derived from enolic acid. Preclinical studies have indicated that meloxicam has potent activity, together with good gastrointestinal and renal tolerability profile. This report summarizes undertaken to compare other NSAIDs in the inhibition of inducible cyclooxygenase (COX-2) inflamed areas (pleurisy rat, peritonitis mice) their influence on activity constitutive (COX-1) stomach, kidney, brain, blood. In pleurisy was twice as tenoxicam, 3 times flurbiprofen, 8 diclofenac, 20 tenidap at inhibiting prostaglandin E2 (PGE2) biosynthesis. model mice, approximately active piroxicam, more than 10 diclofenac suppression PGE Doses sufficient inhibit PGE2 biosynthesis pleural exudate peritoneal had no leukotriene-B4 (LTB4) or leukotriene-C4 (LTC4) content. The effect content rat gastric juice urine weaker piroxicam diclofenac. inhibitor increased concentration brain rats mice (induced by convulsant doses pentetrazole) indomethacin. serum thromboxane-B2 (TXB2) tenoxicam. vivo findings confirm results vitro tests, conducted separately, showing preferentially inhibits COX-2 over COX-1. isoenzyme implicated inflammatory response, whereas COX-1 cytoprotective effects mucosa. Therefore, preferential selectivity for one another, displayed meloxicam, may implications clinical setting terms favorable risk: benefit
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