NSAID zaltoprofen possesses novel anti-nociceptive mechanism through blockage of B2-type bradykinin receptor in nerve endings

Misaki Matsumoto, Makoto Inoue, Hiroshi Ueda

Research output: Contribution to journalArticlepeer-review

Abstract

Zaltoprofen, a propionic acid derivative of non-steroidal anti-inflammatory drugs (NSAIDs), was shown to have more powerful inhibitory effects to bradykinin (BK)-nociception than other NSAIDs. However, the molecular mechanisms underlying this potent analgesia are not yet fully understood. Here we attempted to clarify the molecular mechanism underlying zaltoprofen-induced analgesia on BK-induced nociception by a novel algogenic-induced paw flexion (APF) test in mice. The intraplantar (i.pl.) injection of zaltoprofen at 1 nmol showed strong analgesic action on BK (i.pl.)-induced nociceptive flexor responses, whereas loxoprofen or its active metabolite loxoprofen-SRS did not. Zaltoprofen also inhibited the nociception induced by [Tyr8]-BK, a specific agonist of B2-type BK receptor, but did not affect the nociception by [Lys-des-Arg9]-BK, a specific agonist of B1-type BK receptor. However, zaltoprofen did not affect the substance P-induced nociception, which is mediated by common post-receptor signaling through nociceptive fibers with BK-ones. All these results suggest that NSAID zaltoprofen possesses novel anti-nociceptive mechanism, which inhibits B2-type BK receptor function in nerve endings.

Original languageEnglish (US)
Pages (from-to)249-253
Number of pages5
JournalNeuroscience Letters
Volume397
Issue number3
DOIs
StatePublished - Apr 24 2006
Externally publishedYes

Keywords

  • B2-type BK receptor
  • Bradykinin
  • NSAID
  • Zaltoprofen

ASJC Scopus subject areas

  • Neuroscience(all)

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