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Korean Journal of Anesthesiology 2004;47(6):862-869.
DOI: https://doi.org/10.4097/kjae.2004.47.6.862   
Peripheral Analgesic Effects of NSAIDs and Expressions of Cyclooxygenase-1 and Cyclooxygenase-2 in Acute Arthritic Model in Rats.
Yoon Sook Lee, Ji Yong Park, Hye Ja Lim
Department of Anesthesiology and Pain Medicine, College of Medicine, Korea University, Seoul, Korea. drlimhj@unitel.co.kr
Abstract
BACKGROUND
Theoretically, an NSAID that inhibits COX-2 selectively should decrease inflammation but not influence normal physiologic functions and thus should cause fewer side effects. In the present study, to investigate the extent of peripheral nociception and inflammation of COX-1 and COX-2, diclofenac (non-selective COX inhibitor), SC-560 (selective COX-1 inhibitor) and NS-398 (selective COX-2 inhibitor) were injected intra-articularly on acute arthritic model in rats and COX-1 and COX-2 mRNA expression were measured by reverse transcription polymerase chain reaction (RT-PCR).
METHODS
Arthritis was induced with 2% lambda-carrageenan into the right knee joint cavity under enflurane anesthesia (2-4%). Four and a half hours after the carrageenan injection, diclofenac, SC-560 or NS-398 was injected intra-articularly. The weight loads, diameters of knee joints and body weights were measured. The expressions of COX-1 and COX-2 were investigated in the inflammatory control group by RT-PCR.
RESULTS
The weight loads predominantly increased and the diameters of the knee joints decreased in the diclofenac group, but not in the SC-560 and NS-398 groups. After the induction of arthritis, COX-1 and COX-2 mRNA expression increased with peak response at 9 and 6 hours after the induction, respectively.
CONCLUSIONS
These results suggested that the non-selective COX inhibitor, diclofenac, which was injected intra-articularly, showed effective analgesic and anti-inflammatory effects in acute arthritic rats, and that the expressions of COX-1 and COX-2 mRNA were increased after induction of arthritis.
Key Words: cyclooxygenase; diclofenac; NS-398; peripheral nociception; SC-560


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