Mitchell J A, Evans T W
Unit of Critical Care Medicine, Royal Brompton Hospital, London, UK.
Inflamm Res. 1998 Oct;47 Suppl 2:S88-92. doi: 10.1007/s000110050287.
Cyclooxygenase (COX)-2 is the predominant COX isoform present at sites of inflammation, and produces prostaglandins (PG) that cause swelling and pain. However, in situations where the release of protective PGs by COX-1 has been lost, the induction of COX-2 may compensate and reduce inflammatory responses. This is particularly likely in large blood vessels, where, under physiological conditions, the release of prostacyclin by COX-1, present in the endothelium, is an important component of cardiovascular homeostasis. We, and others, have recently shown that COX-2 can be induced by proinflammatory cytokines in human blood vessels, and also in human airway cells. Moreover, recent data from our group have suggested that in these structures, COX-2 is anti-inflammatory at the level of cellular proliferation, adhesion receptor expression, and cytokine release.
环氧化酶（COX）-2是炎症部位主要存在的COX同工型，可产生导致肿胀和疼痛的前列腺素（PG）。然而，在COX-1释放保护性PG的功能丧失的情况下，COX-2的诱导可能会起到补偿作用并减轻炎症反应。这在大血管中尤为可能，在生理条件下，内皮中存在的COX-1释放前列环素是心血管稳态的重要组成部分。我们和其他人最近表明，COX-2可由促炎细胞因子在人体血管以及人气道细胞中诱导产生。此外，我们小组最近的数据表明，在这些结构中，COX-2在细胞增殖、黏附受体表达和细胞因子释放水平上具有抗炎作用。
