抑制细胞中花生四烯酸的释放作为抗炎皮质类固醇的生化作用。
Inhibition of arachidonic acid release from cells as the biochemical action of anti-inflammatory corticosteroids.
作者信息
Hong S L, Levine L
出版信息
Proc Natl Acad Sci U S A. 1976 May;73(5):1730-4. doi: 10.1073/pnas.73.5.1730.
Abstract
Serum stimulates the production of prostaglandins by transformed mouse fibroblasts. Hydrocortisone (cortisol) inhibits this stimulation. The half-maximal inhibition occurs at 6x10-9 M. Studies with cells labeled with [3H]arachidonic acid in their lipids show that the stimulation by serum results in the release of arachidonic acid from the cellular lipids, mostly phospholipids. Hydrocrotisone inhibits this release but does not inhibit the production of prostaglandins from exogenously supplied arachidonic acid. This inhibition of arachidonic acid release from phospholipids may be the mechanism for the anti-inflammatory action of corticosteroids.
摘要
血清可刺激转化的小鼠成纤维细胞产生前列腺素。氢化可的松（皮质醇）可抑制这种刺激作用。半数最大抑制浓度为6×10⁻⁹ M。对脂质中标记有[³H]花生四烯酸的细胞进行的研究表明，血清刺激会导致花生四烯酸从细胞脂质（主要是磷脂）中释放出来。氢化可的松可抑制这种释放，但不抑制由外源性提供的花生四烯酸生成前列腺素。这种对花生四烯酸从磷脂中释放的抑制作用可能是皮质类固醇抗炎作用的机制。
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