James M J, Penglis P S, Caughey G E, Demasi M, Cleland L G
Rheumatology Unit, Royal Adelaide Hospital, Adelaide, SA, Australia.
Inflamm Res. 2001 May;50(5):249-53. doi: 10.1007/s000110050750.
The eicosanoids, prostaglandin E2 (PGE2) and thromboxane A2 (TXA2), are involved in inflammatory events. TXA2 has potentially pro-inflammatory actions and PGE2 has actions which can be considered both pro- and antiinflammatory. Therefore, it is potentially significant that production of TXA2 and PGE2 by stimulated monocytes have very different time courses. TXA2 synthesis is immediate and dependent on cyclooxygenase Type 1 (COX-1) activity whereas PGE2 synthesis is delayed and dependent on COX-2 activity. These apparent COX-isotype dependencies of TXA2 and PGE2 synthesis can be explained by differences in the affinities of TXA synthase and PGE synthase for the common substrate, PGH2. The findings have implications for the use of NSAIDs and selective COX-2 inhibitors whose actions can increase the monocyte TXA2/PGE2 ratio.
类二十烷酸、前列腺素E2（PGE2）和血栓素A2（TXA2）参与炎症反应。TXA2具有潜在的促炎作用，而PGE2的作用既可以被认为是促炎的，也可以是抗炎的。因此，受刺激的单核细胞产生TXA2和PGE2的时间进程非常不同，这可能具有重要意义。TXA2的合成是即时的，依赖于1型环氧化酶（COX-1）的活性，而PGE2的合成则延迟，依赖于COX-2的活性。TXA2和PGE2合成对COX同工型的这种明显依赖性，可以通过TXA合酶和PGE合酶对共同底物PGH2的亲和力差异来解释。这些发现对非甾体抗炎药（NSAIDs）和选择性COX-2抑制剂的使用具有启示意义，它们的作用可能会增加单核细胞的TXA2/PGE2比值。
