Adelizzi R A
Arthritis and Osteoporosis Center of South Jersey, Stratford 08084-1504, USA.
J Am Osteopath Assoc. 1999 Nov;99(11 Suppl):S7-12.
Nearly 30 years ago, cyclooxygenase (COX) was identified as an enzyme that initiates the biotransformation of arachidonic acid to prostanoids. It is now known that COX exists as two distinct but similar isozymes, COX-1 and COX-2. Prostaglandins (PGs) formed by the enzymatic activity of COX-1 are primarily involved in the regulation of homeostatic functions throughout the body, whereas PGs formed by COX-2 primarily mediate pain and inflammation. Based on structural differences in the active sites of COX-1 and COX-2, a new class of drugs has been developed that specifically inhibits COX-2 but not COX-1 activity. By preserving the synthesis of homeostatic PGs, these specific inhibitors of COX-2 provide the clinical benefits of nonsteroidal anti-inflammatory drugs and minimize the consequences of nonspecific inhibition of PG synthesis.
近30年前,环氧化酶(COX)被鉴定为一种启动花生四烯酸生物转化为前列腺素的酶。现在已知COX以两种不同但相似的同工酶COX-1和COX-2的形式存在。由COX-1的酶活性形成的前列腺素(PGs)主要参与全身稳态功能的调节,而由COX-2形成的PGs主要介导疼痛和炎症。基于COX-1和COX-2活性位点的结构差异,已开发出一类新的药物,其特异性抑制COX-2活性而不抑制COX-1活性。通过保留稳态PGs的合成,这些COX-2特异性抑制剂提供了非甾体抗炎药的临床益处,并将PG合成非特异性抑制的后果降至最低。