Mitchell Jane A, Warner Timothy D
Cardiothoracic Pharmacology, Unit of Critical Care Medicine, National Heart and Lung Institute, Royal Brompton Hospital, Imperial College School of Medicine, Dovehouse Street, London SW3 6LY, UK.
Nat Rev Drug Discov. 2006 Jan;5(1):75-86. doi: 10.1038/nrd1929.
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the formation of prostanoids by the enzyme cyclooxygenase (COX). Work in the past 15 years has shown that COX exists in two forms: COX1, which is largely associated with physiological functions, and COX2, which is largely associated with pathological functions. Heated debate followed the introduction of selective COX2 inhibitors around 5 years ago: do these drugs offer any advantages over the traditional NSAIDs theywere meant to replace, particularly in regard to gastrointestinal and cardiovascular side effects? Here we discuss the evidence and the latest recommendations for the use of selective inhibitors of COX2 as well as the traditional NSAIDs.
非甾体抗炎药（NSAIDs）通过环氧化酶（COX）抑制前列腺素的形成。过去15年的研究表明，COX有两种形式：COX1，主要与生理功能相关；COX2，主要与病理功能相关。大约5年前，选择性COX2抑制剂问世后引发了激烈争论：这些药物相对于它们旨在取代的传统NSAIDs是否具有任何优势，尤其是在胃肠道和心血管副作用方面？在此，我们讨论使用COX2选择性抑制剂以及传统NSAIDs的证据和最新建议。
