The Effect Of Blocking Prostaglandin Synthesis On The Expression Of Endogenous Opioid Peptides In Peripheral Inflammatory Tissues

Cyclooxygenases is a key enzyme for prostaglandin synthesis process. There exsit two isoenzymes:Cyclooxygenase-1(COX-1) and Cyclooxygenase-2(COX-2). COX-1 is a constitutive enzyme can be found in most mammalians; COX-2 is rarely expressed in normal tissues. It is an inducible enzyme and is upregulated at the site of inflammation, suggesting that it is involved inflammatory pain.Endogenous opioids are peptides synthesized in mammal bodies. they produce analgesia or anti-nociception via binding to opioid receptors. Opioid peptides in inflammtory tissues are mainly produced and released by immune cells.This study used behavior, immunohistochemistry, western blot and ELISA and other experimental methods to investigate the effect of COX-2 inhibitor on expression of the endogenous opioid peptides in inflammatory tissue in carrageenan-induced inflammatoin in rats.Results show that i.pl indomethacin (non-selective COX inhibitor) 1h after carrageenan produced dose-dependently hypoalgesia in the second and third day in rats and the content of P-endorphin and the number of P-endorphin-positive cell in the inflammtory site were significantly increased. In addition, i.pl nimesulide (selective COX-2 inhibitor) 1h after carrageenan produces hypoalgesia in the second, third and fourth day in rats and the number of positive cell of P-endorphin in the inflammtory tissue was significantly increased. Moreover, the expression ofμ-receptor in DRG of ipsilateral is also significantly upregulated.The present study shows that inhibition of cyclooxygenases in inflammatory tissue enhanced the expession of endogenous opioid peptides in the inflammtory issue and the expression of opioid receptor in DRG.This provides an evidenceclarifing to illustrate the mechanism of inflammatory pain and exploiting analgesics targeting pronociceptive mediators in the periphery.