Titlebook: New Targets in Inflammation; Inhibitors of COX-2 Nicolas Bazan,Jack Botting,John Vane Conference proceedings 1996 Springer Science+Busines

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Blockade of inflammatory hyperalgesia and cyclooxygenase-2,tentiates the intraplantar effect of IL-l. or carrageenan, suggesting that induction of COX-2 is a limiting process in the development of inflammatory hyperalgesia. Induction of COX-2 is typically inhibited by corticosteroids. In our system IL-1. -induced hyperalgesia is inhibited by dexamethasone t

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Brain COX-2 in experimental models of epilepsy and stroke: signalling pathways leading to enhanced s. BN 50730, an intracellular PAF antagonist., blocks PAF-induced COX-2 expression. We therefore tested the effectiveness of BN 50730 in blocking induction of COX-2 mRNA and protein expression in vivo. The two models used were focal cerebral ischaemia using the suture model of middle cerebral artery

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New highly selective cyclooxygenase-2 inhibitors,ning the protein in the endoplasmic reticulum. The main significant difference between COX-2 and COX-1 is that COX-2 can be induced transiently over a >50-fold range by a variety of agents, including cytokines, phorbol esters, hormones, serum and lipopolysaccharide. This induction can be inhibited b

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Clinical experience with meloxicam, a selective COX-2 inhibitor,e NSAIDs are selective for COX-1 or are equipotent against both COX-1 and COX-2. NSAIDs such as meloxicam, which are more selective for COX-2 than for COX-1, have been developed and are efficacious in the treatment of rheumatic disease. Drugs which are highly selective for COX-2 are presently being

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in clinical trials gastric and renal toxicities are less. Highly selective COX-2 inhibitors, perhaps designed with knowledge of the crystal structures of COX-I and COX-2, are also available. Other experimental studies, including those in animals lacking effective genes for COX-lor COX-2 and in experimental c978-94-010-6265-7978-94-011-5386-7

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