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Prostaglandin (PG) E 2  and PGI 2  are essential to hyperalgesia in inflammatory tissues. These prostaglandins are produced from arachidonic acid, which is cleaved from membrane phospholipids by the action of phospholipase A 2  (PLA 2 ). Which isozyme of PLA 2  is responsible for the cleavage of arachidonic acid and the production of prostaglandins essential to inflammation-induced hyperalgesia is not clear. In this study, we examined the effects of two PLA 2  isozyme-specific inhibitors on carrageenan-induced production of PGE 2  and PGI 2  in rat hind paw and behavioral nociceptive response to radiant heat. Local administration of bromoenol lactone (BEL), an inhibitor of calcium-independent PLA 2  (iPLA 2 ), significantly reduced carrageenan-induced elevation of prostaglandins in the inflamed foot pad 3 h after injection. It also ameliorated the hyperalgesic response between 1 h and 3 h after carrageenan injection. On the other hand, AACOCF 3 , an inhibitor of cytosolic PLA 2 , suppressed neither prostaglandin production nor the hyperalgesic response. BEL did not suppress the mRNA levels of iPLA 2   β , iPLA 2   γ , cyclooxygenase-2, microsomal prostaglandin E synthase, prostaglandin I synthase, or proinflammatory cytokines in the inflamed foot pad, indicating that BEL did not suppress inflammation itself. These results suggest that iPLA 2  is involved in the production of prostaglandins and hyperalgesia at the inflammatory loci.

mediators of inflammation

Bromoenol Lactone, an Inhibitor of Calcium-Independent Phospholipase A<sub>2</sub>, Suppresses Carrageenan-Induced Prostaglandin Production and Hyperalgesia in Rat Hind Paw

Bromoenol Lactone, an Inhibitor of Calcium-Independent Phospholipase A2, Suppresses Carrageenan-Induced Prostaglandin Production and Hyperalgesia in Rat Hind Paw

Bromoenol Lactone, an Inhibitor of Calcium-Independent Phospholipase A₂, Suppresses Carrageenan-Induced Prostaglandin Production and Hyperalgesia in Rat Hind Paw