Abstract
The synthetic opioid peptide (D-Ala2) methionine enkephalinamide (DAMEA) was reported to be an extremely potent inhibitor of the "respiratory burst" of polymorphonuclear neutrophils (PMNs). In the present paper the activity of DAMEA was investigated in the PMA-induced mouse ear edema since there is strong evidence that reactive oxygen species (ROS) are involved in the pathogenesis of this inflammatory reaction. DAMEA inhibited PMA-induced mouse ear edema in a dose-dependent manner between 10(-6) and 10(-9) mol/ear. The well-known anti-inflammatory activity of narcotic analgesics could be explained partly by an inhibition of ROS production.
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