Anti-allodynic and anti-hyperalgesic activity of (±)-licarin A in neuropathic rats via NO-cyclic-GMP-ATP-sensitive K+ channel pathway.

Abstract

The study aimed to examine the effect of intraperitoneal and intrathecal (±)-licarin A in neuropathic pain induced by L5 and L6 spinal nerve ligation (SNL) in male Wistar rats and the possible involvement of the NO-cGMP-ATP-sensitive K+ channel pathway. Neuropathic pain signs (allodynia and hyperalgesia) were evaluated on postoperative Day 14 using von Frey filaments. Single intraperitoneal (0.01, 0.1, 1, and 10 mg/kg) and intrathecal (0.01, 0.1, 1, and 10 µg/rat) administration of (±)-licarin A improved allodynia and hyperalgesia. The (±)-licarin A-induced anti-allodynic and anti-hyperalgesic activity was prevented by the intrathecal injection of l-NAME (100 µg/rat; nonselective nitric oxide synthase inhibitor), ODQ (10 µg/rat; guanylate cyclase inhibitor), and glibenclamide (50 µg/rat; adenosine triphosphate (ATP)-sensitive K+ channel blocker). The data suggest that (±)-licarin A exerts its anti-allodynic and anti-hyperalgesic activity by activating the NO-cGMP-ATP-sensitive K+ channel pathway.