Interleukin-2-induced antinociception in morphine-insensitive rats.
Abstract
AIM: To investigate interleukin-2-induced antinociception in morphine-insensitive
rats.
METHODS: Paw withdrawal latencies (PWL) to noxious radiant heat were taken as the
measurement of pain threshold.
RESULTS: Intraplantar injection of human recombinant interleukin-2 (1.5 x10(4) U)
significantly increased PWL in normal rats. PWL was also markedly increased by
IL-2 in 45-d-post-complete Freund's adjuvant (CFA)-treated rats, which have been
proven morphine-insensitive. IL-2-induced antinociception in CFA-treated rats
were significantly lower than that in normal rats. IL-2-induced antinociception
was partially blocked by naloxone (1 mg/kg, ip) in normal rats but remained
unchanged in CFA group.
CONCLUSION: IL-2-induced antinociception is partially mediated by mu-opioid
receptors. Therapeutic applications of IL-2 may also be expanded to relieve
morphine-insensitive pain.
Keywords:
rats.
METHODS: Paw withdrawal latencies (PWL) to noxious radiant heat were taken as the
measurement of pain threshold.
RESULTS: Intraplantar injection of human recombinant interleukin-2 (1.5 x10(4) U)
significantly increased PWL in normal rats. PWL was also markedly increased by
IL-2 in 45-d-post-complete Freund's adjuvant (CFA)-treated rats, which have been
proven morphine-insensitive. IL-2-induced antinociception in CFA-treated rats
were significantly lower than that in normal rats. IL-2-induced antinociception
was partially blocked by naloxone (1 mg/kg, ip) in normal rats but remained
unchanged in CFA group.
CONCLUSION: IL-2-induced antinociception is partially mediated by mu-opioid
receptors. Therapeutic applications of IL-2 may also be expanded to relieve
morphine-insensitive pain.