The release of prostaglandin and slow reacting substance from mouse macrophages

Abstract

The release of PGE and SRS from mouse resident peritoneal macrophages has been studied after various stimuli. Both substances were released, in most cases, conjointly and were inhibited by drugs in a similar manner. IntroductionMacrophages release large amounts of prostaglandins in response to certain phagocytic stimuli [1] reflecting the high content of arachidonic acid in the phospholipids of their membranes [21. Mouse macrophages exposed to zymosan release a slow reacting substance (SRS) similar to leuko triene C 4 [31. We report the effects of various particulate and soluble stimuli on the release of PGE and SRS from mouse macrophages and the modulation of release by drugs.

Local anti-inflammatory activities of tixocortol 21-pivalate, inhibition of prostaglandins and leukotrienes synthesis, in carrageenin-induced pleurisy. Reversion of effects by RU 486

“…The present data indicate that local effects of drugs on LT as well as PG synthesis can be investigated simultaneously with exudate volume and cell migration. Glucosteroids have been claimed to indirectly inhibit LT production through phospholipase A2 inhibition [18] but only few data have been published on LT synthesis inhibition by glucosteroids except in lung, in mouse macrophages and in human basophils [19][20]. In addition to the already reported inhibition of PGE2 synthesis after oral administration, LTC4/D4 synthesis was also found inhibited by glucosteroids in this model.…”