D-penicillamine effects on prostanoid production in adherent rheumatic synovial cells in primary culture.
The effect of D-penicillamine (DPA) on immunoreactive prostanoid concentrations was studied in a primary culture of adherent synovial cells from patients suffering from rheumatoid arthritis (RA). DPA in clinically achievable concentrations increased the levels of prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) and reduced those of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) synthetized from endogenous substrate. The capacity for PGE2 and 6-keto-PGF1 alpha production in the presence of exogenous arachidonic acid was decreased by DPA. These effects may be connected with the antirheumatic and immunosuppressive action of DPA.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000328:Adult; D001172:Arthritis, Rheumatoid / Q000378:metabolism*; D002478:Cells, Cultured; D015237:Dinoprost; D015232:Dinoprostone; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010396:Penicillamine / Q000494:pharmacology*; D011453:Prostaglandins / Q000378:metabolism*; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D013583:Synovial Membrane / Q000187:drug effects / Q000378:metabolism*; D013929:Thromboxane B2 / Q000378:metabolism*
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D010396:Penicillamine; D015232:Dinoprostone