Abramson S, Edelson H, Kaplan H, Given W, Weissmann G
Semin Arthritis Rheum. 1983 Aug;13(1 Suppl 1):148-53. doi: 10.1016/0049-0172(83)90035-5.
The activation of the polymorphonuclear leukocyte (PMN) in rheumatoid arthritis produces toxic products that include lysosomal enzymes, stable prostaglandins, and leukotrienes and causes the release of superoxide anion. These products produce the inflammatory response, damage cell membranes, and degrade hyaluronic acid. The inhibition of prostaglandin synthetase by NSAIDs does not, by itself, account for their effectiveness in preventing inflammation in rheumatoid arthritis. In vivo and in vitro experiments were conducted to determine if NSAIDs also exert an effect on neutrophil activation. The NSAIDs tested inhibited discrete PMN functions dependent upon the stimulus tested. The antiinflammatory effects of NSAIDs cannot be entirely explained by their inhibition of prostaglandin synthetase and may, in part, be due to other direct effects upon inflammatory cell activation.
类风湿关节炎中多形核白细胞（PMN）的激活会产生包括溶酶体酶、稳定的前列腺素和白三烯在内的毒性产物，并导致超氧阴离子的释放。这些产物引发炎症反应，损伤细胞膜并降解透明质酸。非甾体抗炎药（NSAIDs）对前列腺素合成酶的抑制作用本身并不能解释它们在预防类风湿关节炎炎症方面的有效性。进行了体内和体外实验以确定NSAIDs是否也对中性粒细胞激活有作用。所测试的NSAIDs抑制了取决于所测试刺激的离散PMN功能。NSAIDs的抗炎作用不能完全通过其对前列腺素合成酶的抑制来解释，可能部分归因于对炎症细胞激活的其他直接作用。
