Pairet M, Engelhardt G
Department of Biological Research, Boehringer Ingelheim Research Laboratories, Biberach an der Riss, Germany.
Fundam Clin Pharmacol. 1996;10(1):1-17. doi: 10.1111/j.1472-8206.1996.tb00144.x.
The discovery of an inducible isoform of cyclooxygenase (COX-2) requires a refinement of the theory that inhibition of cyclooxygenase activity explains both therapeutic and side effects of non-steroidal anti-inflammatory drugs (NSAIDs). Indeed, new pharmacological results suggest that COX-2 inhibition provides the therapeutic (ie, anti-inflammatory) activity of NSAIDs, whereas inhibition of constitutive COX-1 is responsible for their gastric and renal side effects as well as for their antithrombotic activity. However, a role of COX-1 in inflammation cannot be excluded. Furthermore, the functional relevance of COX-2 expression and induction in various tissues warrants further investigation. These studies should help in predicting potential adverse effects as well as new indications for selective COX-2 inhibitors.
环氧化酶（COX-2）诱导型同工型的发现，需要对以下理论进行完善：即环氧化酶活性的抑制可解释非甾体抗炎药（NSAIDs）的治疗作用和副作用。的确，新的药理学结果表明，COX-2抑制作用产生NSAIDs的治疗（即抗炎）活性，而组成型COX-1的抑制作用则导致其胃部和肾脏副作用以及抗血栓活性。然而，不能排除COX-1在炎症中的作用。此外，COX-2在各种组织中的表达和诱导的功能相关性值得进一步研究。这些研究应有助于预测选择性COX-2抑制剂的潜在不良反应以及新适应症。
