Diethylcarbamazine inhibits endothelial and microfilarial prostanoid metabolism in vitro

摘要: Diethylcarbamazine (DEC) rapidly lowers the number of microfilariae in peripheral circulation. The mechanism action is unknown, but may involve alterations arachidonic acid metabolism vascular tissues. We studied effects DEC on by bovine pulmonary arterial endothelium monolayers, human platelets andBrugia malayi microfilariae. at a concentration 2.5 μM, level achieved vivo, decreased prostacyclin, prostaglandin E2 and throm☐ane B2 release from endothelial monolayers 78% (P<0.001), 57% (P=0.05), 75% (P<0.05), respectively. High-pressure liquid chromatography extracts incubated with showed similar inhibition these cyclooxygenase pathway products, exposure to drug did not result formation new eicosanoids. inhibit phospholipase A2-dependent arachidonate membrane stores, whereas H2 synthase activity (cyclooxygenase, EC 1.14.99.1) was reduced degree that effected acetylsalicylic acid. Microfilarial platelet synthesis products also DEC. These data suggest which circulation part its host parasite eicosanoid production.