Goppelt-Struebe M
Universität Erlangen-Nürnberg, Erlangen, Germany.
Biochem Pharmacol. 1997 May 15;53(10):1389-95. doi: 10.1016/s0006-2952(97)00018-x.
The anti-inflammatory properties of glucocorticoids are attributed in part, to their interference with prostaglandin synthesis. Phospholipases A2 and cyclooxygenases, the key enzymes of prostaglandin biosynthesis, are targets of glucocorticoid action; the molecular mechanisms, however, are not yet understood in detail. Obviously, glucocorticoids can act at different levels of gene regulation depending on cell type and inducing stimulus. The current knowledge of glucocorticoid interference with phospholipase A2 and cyclooxygenase expression is summarized. In comparison with other nonsteroidal anti-inflammatory drugs, glucocorticoids are unique inasmuch as they also inhibit cytokine synthesis and expression of other inflammation-related enzymes. Based on a more detailed understanding of glucocorticoid action, it may be possible to therapeutically exploit the anti-inflammatory effects and at the same time avoid the unwanted metabolic actions of these steroids.
糖皮质激素的抗炎特性部分归因于它们对前列腺素合成的干扰。磷脂酶A2和环氧化酶是前列腺素生物合成的关键酶，是糖皮质激素作用的靶点；然而，其分子机制尚未完全明确。显然，根据细胞类型和诱导刺激，糖皮质激素可在基因调控的不同水平发挥作用。本文总结了目前关于糖皮质激素对磷脂酶A2和环氧化酶表达干扰的认识。与其他非甾体抗炎药相比，糖皮质激素的独特之处在于它们还能抑制细胞因子的合成以及其他炎症相关酶的表达。基于对糖皮质激素作用更详细的了解，有可能在治疗上利用其抗炎作用，同时避免这些类固醇不必要的代谢作用。
