Antipyretic analgesics inhibit prostaglandin release from astrocytes and macrophages similarly

Abstract

The effect of acid and non-acid antipyretic analgesics on prostaglandin (PG) release from cultured mouse astrocytes and peritoneal macrophages was investigated in order to test the hypothesis that the non-acid compounds are more potent inhibitors of PG formation in brain than in peripheral tissues. Stimulation of the cells by the divalent cation ionophore A 23187 (10 −6 mol/1) induced PG release from astrocytes and macrophages (mainly PGD 2 and PGE 2, respectively). This PG release was inhibited by acetylsalicylic acid (10 −5 – 10 −6 mol/1) and indomethacin (10 −6 – 10 −9 mol/1) but also by high concentrations (10 −3 – 10 −5 mol/1) of the non-acid compounds 4-methyl-aminophenazone, the main active metabolite of dipyrone (metamizol), and acetaminophen (paracetamol). No difference was found in the inhibitory potency of the drugs in astrocytes and macrophages, suggesting that a specific sensitivity of brain cells toward non-acid antipyretic analgesics does not contribute to their analgesic effect.