Role of l-arginine/SNAP/NO/cGMP/KATP channel signalling pathway in antinociceptive effect of α-terpineol in mice.

Abstract

The main purpose of this study was to assess the role of l-arginine/SNAP/NO/cGMP/KATP channel pathway in analgesic effects of α-terpineol in mice. Male NMRI mice were pretreated intraperitoneally with NO precursor (l-arginine, 100mg/kg), NO synthase inhibitor (l-NAME, 30mg/kg), NO donor (SNAP, 1mg/kg), guanylyl cyclase inhibitor (methylene blue, 20mg/kg), PDE inhibitor (sildenafil, 0.5mg/kg), KATP channel blocker (glibenclamide, 10mg/kg) and naloxone (2mg/kg) 20min before the administration of α-terpineol. The formalin test was performed 20min after the administration of α-terpineol, and nociceptive responses of mice were recorded during 30min. A significant and dose-dependent antinociception was produced by α-terpineol (40 and 80mg/kg) in both the phases of formalin test. The antinociceptive effect of α-terpineol was significantly potentiated by l-arginine in the second phase while significantly antagonized by l-NAME in both phases of formalin test. Also, SNAP and sildenafil non-significantly enhanced-while methylene blue significantly diminished-the antinociceptive effect of α-terpineol in both phases of formalin test. Glibenclamide significantly reversed the α-terpineol-induced antinociception, indicating the involvement of KATP channels in antinociceptive effect of α-terpineol. These results indicate that the antinociceptive effect of α-terpineol is mediated through l-arginine/SNAP/NO/cGMP/KATP channel pathway.