Non-steroidal anti-inflammatory drugs (NSAIDs) are generally attributed to suppression cyclooxygenase enzymes, leading to decreased products of the arachidonic acid cascade. Since the discovery of two isoenzymes of cyclooxygenase, inhibition of cyclooxygenase-2 has been suggested to be responsible for therapeutic effects of NSAIDs without side effects. In the present study, to investigate the extent to peripheral nociception and inflammation of cyclooxygenase-1 and cyclooxygenase-2, diclofenac (non-selective inhibitor), SC-560 (selective cyclooxygenase-1 inhibitor) and NS-398 (selective cyclooxygenase-2 inhibitor) are injected intra-articularly on acute arthritic model in rats.

Arthritis was induced with 2% λ-carrageenan (suspended in 50 µl normal saline) into the right knee joint cavity under enflurane anesthesia (2-4%). Before and after the injection, rats were allowed to walk freely through a pathway constructed to record weight load by means of 8 weight sensors (strain gauge type) attached to 8 plates which function independently. The weight load, diameter of both knee joints and weight of rat were measured at each test. At 4 hours and 30 minutes, diclofenac, SC-560 and NS-398 dissolved in 10% dimethyl sulfoxide were injected intra-articularly (50 µg/50 µl).

The weight loads increased in diclofenac group at 6 and 9 hours and in NS-398 group at 24 and 48 hours after induction of arthritis. The diameter ratio decreased in diclofenac group at 12 hours after induction of arthritis.

These results suggest that peripheral nociception and inflammation in acute model of arthritis in rats are likely related with both cyclooxygenase-1 and cyclooxygenase-2 pathways.