ABSTRACT
Non-steroidal anti-inflammatory drugs (NSAIDS) inhibit cyclooxy- genase (COX), the enzymes that are responsible for prostaglandin production [1]. There are two isoforms, COX-1 which is constitutively expressed, and COX-2 which is inducible. NSAIDS are widely used for their analgesic, antipyretic and anti-inflammatory properties however despite their therapeutic effectiveness, their use has been widely scruti- nized due to their tendency to produce side effects. Since prostaglandins protect the gastrointestinal tract and are important in platelet aggrega- tion, NSAID reduction of prostanoid production increases the risk of gastrointestinal ulceration and bleeds. Due to the toxic effects of NSAIDs such as diclofenac on gastrointestinal mucosa, COX-2 selective drugs such as celecoxib were developed.
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Date of publication: 11 January 2016; Life Sciences
Author information: Mire Zloh (1); Noelia Perez-Diaz (1); Leslie Tang (1); Pryank Patel (1); & Louise S. Mackenzie (1)
(1) Life and Medical Sciences, University of Hertfordshire, Hatfield AL10 9AB, UK