Newman S P, Flower R J, Croxtall J D
Department of Biochemical Pharmacology, William Harvey Research Institute, Medical School of St. Batholomew's Hospital, London, UK.
Biochem Biophys Res Commun. 1994 Jul 29;202(2):931-9. doi: 10.1006/bbrc.1994.2019.
A549 cells grown under serum free conditions do not express cyclooxygenase 2 (cox 2). However, addition of IL-1 beta results in the induction of cox 2 in a time and dose dependent manner; actinomycin D completely blocks this induction. Dexamethasone completely suppressed the induction of cox 2 only if present during the first 3.5h of IL-1 beta treatment but not if added after 3.5h. Treatment with a neutralising monoclonal antibody (1A, Biogen) specific to lipocortin-1 failed to reverse this inhibition by dexamethasone. However, using this same antibody we were able to reverse completely the effects of dexamethasone on the suppression of PGE2 release. These observations support the idea that glucocorticoids directly regulate cox 2 expression at the transcriptional level and this phenomenon is not mediated by lipocortin-1.
在无血清条件下培养的A549细胞不表达环氧化酶2（COX 2）。然而，添加白细胞介素-1β会以时间和剂量依赖的方式诱导COX 2的表达；放线菌素D完全阻断这种诱导作用。仅在白细胞介素-1β处理的前3.5小时存在时，地塞米松才能完全抑制COX 2的诱导，而在3.5小时后添加则不能。用针对脂皮质蛋白-1的中和单克隆抗体（1A，Biogen）处理未能逆转地塞米松的这种抑制作用。然而，使用相同的抗体，我们能够完全逆转地塞米松对前列腺素E2释放抑制的作用。这些观察结果支持这样一种观点，即糖皮质激素在转录水平直接调节COX 2的表达，并且这种现象不是由脂皮质蛋白-1介导的。
