The present study was undertaken to examine whether and what type of interaction occurs between a synthetic glucocorticoid, dexamethasone (DEX) and an opioid peptide, met-enkephalin (MENK) upon superoxide anion (O2-) release from human polymorphonuclear cells (PMN). MENK (10(-8) M) abolished suppressed O2- release from PMNs treated with 10(-7) M DEX. This was the case in unstimulated but not in PMNs stimulated with PMA. The effect of MENK was mediated through pertussis-toxin (PTX) sensitive G-protein and since it was abolished by H7 probably involves protein kinase C (PKC) as a second messenger system. Thus, MENK can abolish DEX induced suppression of O2- release from human PMNs possibly through the interaction of second messenger pathways.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine Dexamethasone