Jachak Sanjay M
National Institute of Pharmaceutical Education and Research, Department of Natural Products, Sector 67, SAS Nagar, Punjab 160 062, India.
Curr Opin Investig Drugs. 2007 May;8(5):411-5.
NSAIDs and selective COX-2 inhibitors reduce the formation of prostanoids, particularly PGE2, to diminish inflammation. However, these drugs exhibit toxicities, including gastrointestinal bleeding and myocardial infarction. In cells, arachidonic acid is converted to PGE2 by the action of COX enzymes and terminal PGE synthase. This review discusses the problems associated with selective COX-2 inhibitors and describes the microsomal PGE synthase-1 enzyme, its regulation and role in inflammatory diseases, its known inhibitors, and its potential as an alternative target for the development of novel anti-inflammatory agents.
非甾体抗炎药（NSAIDs）和选择性环氧化酶-2（COX-2）抑制剂可减少前列腺素的生成，尤其是前列腺素E2（PGE2），从而减轻炎症。然而，这些药物存在毒性，包括胃肠道出血和心肌梗死。在细胞中，花生四烯酸在COX酶和末端PGE合酶的作用下转化为PGE2。本综述讨论了与选择性COX-2抑制剂相关的问题，并描述了微粒体PGE合酶-1酶、其调节及其在炎症性疾病中的作用、其已知抑制剂，以及其作为新型抗炎药开发替代靶点的潜力。
