Inhibition of prostaglandin synthesis in intact cells by paracetamol (acetaminophen)

摘要: Despite its wide use, the mechanism of action paracetamol (acetaminophen) is uncertain. It commonly stated to be a weak inhibitor synthesis prostaglandins (PGs) by prostaglandin H synthases (COX-1 and COX-2) but inhibits PGs in stimulated cultured cells with IC50 values ranging from 4 200 μM. Paradoxically, it generally stimulates PG production broken cell preparations. Here we show that human rheumatoid synoviocytes during stimulation interleukin1β (0.1ng/ml) for 18 h. Paracetamol inhibited both PGE2 PGF2αwith median 7.2 4.2 μM respectively, without affecting or level constitutive enzyme, COX-1 interleukin-1β mediated induction COX-2 cytosolic phospholipase A2-α (cPLA2-α). These data indicate suppresses delayed direct modulation cPLA2-α /COX-2 pathway at therapeutic concentrations. substituted phenol effects on are very similar those other phenols. should considered inhibit although cause selectivity; analgesic antipyretic antiplatelet anti-inflammatory unknown.