Inhibition by glucocorticoids of prostaglandin release from adipose tissue in vitro.
1 When rabbit chopped adipose tissue was incubated with a lipolytic agent (adrenocorticotrophic hormone, ACTH1-24, 0.1 microng/ml) in Krebs solution, prostaglandin E2 was formed in the tissue and about the same amount was found in the medium. 2 In the presence of indomethacin (1 microng/ml) the appearance of prostaglandin E2 was almost abolished both in the tissue and in the medium. 3 When the incubation was carried out in the presence of hydrocortisone or betamethasone (1-10 microng)ml) the concentration of prostaglandin E2 leaking or carried into the medium was significantly reduced, whereas that remaining in the tissue was significantly increased. This action of the steroids was not reversed by increasing substrate (arachidonic acid) concentration in the medium. 4 The steroids did not affect lipolysis, nor did they influence prostaglandin metabolism since such activity was not detectable in the adipose tissue. 5 Anti-inflammatory steroids therefore did not reduce prostaglandin formation but increased the tissue/medium ratio, which supports the view that they inhibit the release of prostaglandins after these have been synthesized.
D000273:Adipose Tissue / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D001623:Betamethasone / Q000494:pharmacology*; D002855:Chromatography, Thin Layer; D003864:Depression, Chemical; D005260:Female; D005990:Glycerol / Q000378:metabolism; D006854:Hydrocortisone / Q000494:pharmacology*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D050356:Lipid Metabolism; D011458:Prostaglandins E / Q000378:metabolism*; D011817:Rabbits
D001095:Arachidonic Acids; D011458:Prostaglandins E; D000324:Adrenocorticotropic Hormone; D001623:Betamethasone; D005990:Glycerol; D006854:Hydrocortisone; D007213:Indomethacin