Tam S, Hong S C, Levine L
J Pharmacol Exp Ther. 1977 Oct;203(1):162-8.
Anti-inflammatory steroids inhibit the serum-stimulated prostaglandin synthesis and release of [3H]arachidonic acid by methylcholanthrene-transformed mouse fibroblast, MC5-5. The half-maximal concentration for inhibition of both effects parallels the relative anti-inflammatory potencies of these steroids. The fatty acid cyclooxygenase activities of microsomal fractions isolated from cells that had been pretreated with dexamethasone were similar to the activities of microsomal fractions isolated from untreated cells. Intracellular as well as extracellular levels of prostaglandins in dexamethasone inhibited cells were decreased. The anti-inflammatory steroids seem to be blocking deacylation of the phospholipids or transport of the arachidonic acid, after deacylation to the cyclooxygenase.
抗炎类固醇可抑制血清刺激的甲基胆蒽转化小鼠成纤维细胞MC5-5合成前列腺素并释放[3H]花生四烯酸。抑制这两种效应的半数最大浓度与这些类固醇的相对抗炎效力相当。从用地塞米松预处理过的细胞中分离得到的微粒体部分的脂肪酸环氧化酶活性,与从未经处理的细胞中分离得到的微粒体部分的活性相似。地塞米松处理的细胞中,细胞内和细胞外的前列腺素水平均降低。抗炎类固醇似乎是在磷脂脱酰基作用或花生四烯酸脱酰基后向环氧化酶的转运过程中发挥阻断作用。