INDUCTION OF PROSTACYCLIN FORMATION BY SODIUM N-BUTYRATE IN A CLONED EPITHELIAL LIVER-CELL LINE

  • 1 January 1981
    • journal article
    • research article
    • Vol. 664  (2) , 278-290
Abstract
The effect of sodium n-butyrate on prostaglandin synthesis in cultured cells was examined. Exposure of BC-90 cells, a clone of an epithelial rat liver cell line, to 1 mM sodium n-butyrate for 40 h induced prostacyclin production. Prostacyclin synthesis was proved by demonstrating production of labeled 6-ketoprostaglandin F1.alpha. by treating [14C]arachidonic acid pre-labeled cells with Ca ionophore A23187 [calcimycin], production of unstable substance that inhibited ADP-induced platelet aggregation, and conversion of [14C] arachidonic acid to 6-ketoprostaglandin F1.alpha. in homogenates of n-butyrate-treated cells. Untreated control cells showed negligible prostaglandin synthesis. Untreated cell homogenates did not convert [14C]arachidonic acid to any prostaglandins, but they converted [14C]prostaglandin H2 to prostacyclin. Induction of prostacyclin production by n-butyrate was also demonstrated with cells that were treated with acetylsalicylic acid before n-butyrate treatment in acetylsalicylic acid-free medium. Incorporation of [3H]acetylsalicylic acid by sodium n-butyrate-treated cells increased in accordance with treatment time, while that of untreated cells did not change during culture. There was no difference in the phospholipase A2 activities of n-butyrate-treated and -untreated cells. The possibility that n-butyrate induced prostacyclin in BC-90 cells through induction of fatty acid cyclooxygenase activity is discussed.