[Effect of SIN-1 on the synthesis of leukotrienes in human polymorphonuclear cells].
Leukotriene (LT) synthesis triggered with ionophore A23187 or inflammatory stimuli (PAF, fMLP) in human polymorphonuclear leukocytes (PMNL) was markedly decreased by SIN-1, an active metabolite of molsidomine. This inhibition occurred in the absence or in the presence of exogenous arachidonic acid (AA). These results suggest that SIN-1 inhibited both the release of AA from membrane phospholipids and the 5-lipoxygenase activity in human PMNL. Molsidomine was without any effect on LT formation.
D001095:Arachidonic Acids / Q000378:metabolism*; D006801:Humans; D017572:Leukotriene A4; D007975:Leukotriene B4 / Q000378:metabolism*; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009504:Neutrophils / Q000378:metabolism*
D001095:Arachidonic Acids; D017572:Leukotriene A4; D007975:Leukotriene B4; C002385:linsidomine; D008981:Molsidomine
Effet du SIN-1 sur la synthèse de leucotriènes dans les polymorphonucléaires humains.