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Abstract

Inflammation is the response of living tissues to injury. It involves a complex battery of enzyme activation, mediator release, extravasation of fluid, cell migration, tissue breakdown and repair. This overview will concentrate on the actions of anti-inflammatory drugs, with special reference to the prostaglandin system. This system is activated by phospholipase A2, which liberates arachidonic acid, the substrate for cyclooxygenase (COX or PGH2 synthase). This leads to an increased production of prostaglandins (Figure 1). Prostaglandin E2 is the predominant eicosanoid detected in inflammatory conditions in man ranging from experimental acute oedema and sunburn through to chronic arthritis. Because inflammation is one of the few conditions in which PGE2 is a major product of COX it is possible that the process of inflammation directs the enzymic pathway towards this product. A second enzyme, 5-lipoxygenase converts arachidonic acid to the leukotrienes1, which are important mediators of asthma, but this aspect will not be discussed here.

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© 1996 Kluwer Academic Publishers and William Harvey Press

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Vane, J.R., Botting, R.M. (1996). Overview — mechanisms of action of anti-inflammatory drugs. In: Vane, J., Botting, J., Botting, R. (eds) Improved Non-Steroid Anti-Inflammatory Drugs: COX-2 Enzyme Inhibitors. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-9029-2_1

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  • DOI: https://doi.org/10.1007/978-94-010-9029-2_1

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