Abstract
Anti-inflammatory glucocorticoids inhibit prostaglandin (PG) biosynthesis by preventing arachidonic acid release from phospholipids. As in other cells, this steroid action depends on receptor occupation and de novo' protein/RNA biosynthesis. We have shown in guinea pig perfused lungs and rat peritoneal leukocytes that the effect of steroids on PG generation is mediated by a second messenger'. This inhibitory factor (which we have named macrocortin') is an intracellular polypeptide whose release and synthesis are stimulated by steroids.
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