Inhibition of mast cell-dependent anaphylaxis by sodium salicylate

Sodium salicylate (NaSal) is a commonly used agent with a wide pharmacologi cal spectrum. The objective of the present study was to investigate the eff ect of NaSal on anaphylaxis. NaSal (10(-1) and 1 mM) significantly inhibite d systemic anaphylaxis induced by compound 48/80 in rats. NaSal also signif icantly inhibited local anaphylaxis activated by anti-dinitrophenyl (DNP) i mmunoglobulin E(IgE). NaSal (10(-1) and 1 mM) significantly inhibited hista mine release from rat peritoneal mast cells (RPMC) activated by compound 48 /80 or anti-DNP IgE. Northern-blot analysis demonstrated that a significant ly reduced level of the mRNA of L-histidine decarboxylase was expressed in mast cells treated with NaSal, compared with that without NaSal. NaSal (10( -2) and 10(-1) mM) had a significant inhibitory effect on anti-DNP IgE-indu ced tumour necrosis factor-alpha secretion from RPMC. The level of cyclic A MP in RPMC, when NaSal (1 mM) was added, transiently and significantly incr eased about sixfold compared with that of basal cells. These results sugges t a possible use of NaSal in managing mast cell-dependent anaphylaxis.