Goodwin J S, Ceuppens J L
Semin Arthritis Rheum. 1983 Aug;13(1 Suppl 1):134-43. doi: 10.1016/0049-0172(83)90033-1.
Nonsteroidal antiinflammatory drugs (NSAID) have been thought to act by inhibiting the production of prostaglandins. Until recently, prostaglandins have been considered to be mainly proinflammatory compounds, responsible for pain, increased blood flow, and edema. It has more lately been realized that prostaglandins, particularly PGE2, have important immunoregulatory properties. Thus NSAID, by inhibiting PGE2 production, modulate immune responses in vitro and in vivo. One or more of these immunomodulating effects of NSAID may play a role in their efficacy as arthritis medications. The purpose of this paper is to review the immunologic role of PGE2 and the immunologic effects of NSAID.
非甾体抗炎药（NSAID）被认为是通过抑制前列腺素的产生来发挥作用的。直到最近，前列腺素一直被认为主要是促炎化合物，负责疼痛、血流量增加和水肿。最近人们才意识到，前列腺素，尤其是前列腺素E2（PGE2），具有重要的免疫调节特性。因此，NSAID通过抑制PGE2的产生，在体外和体内调节免疫反应。NSAID的这些免疫调节作用中的一种或多种可能在其作为关节炎药物的疗效中发挥作用。本文的目的是综述PGE2的免疫作用以及NSAID的免疫效应。
