Abstract
The effect of piroxicam on polymorphonuclear neutrophils (PMN) functions induced by several stimuli was evaluated in vitro. Preincubation of rabbit or human PMN with piroxicam inhibited the cellular responses elicited by N-formyl-methionyl-leucyl-phenylalanine (FMLP) such as superoxide anion (O2-) generation, granule enzyme release and chemotaxis. The effectiveness of piroxicam on each response was superior to those of indomethacin and ibuprofen. Also when either concanavalin A, zymosan-treated serum or ionophore A23187 was used as stimuli, piroxicam inhibited O2- generation of PMN. The inhibitory effect of piroxicam on FMLP-induced O2- generation was dependent on the concentration of stimuli and was reversed by increasing the extracellular calcium concentration. In addition, piroxicam had no effect on the activity of a chymotrypsin-like esterase, N-acetyl-phenylalanine-beta-naphthyl esterase, isolated from rabbit PMN. These results suggest that at least some of the anti-inflammatory effects of piroxicam may be mediated by affecting PMN functions, and the inhibition of O2- generation of PMN by piroxicam may be related to its capacity to modulate the association of calcium with these cells.
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