Anti-allodynic effect of mangiferin in neuropathic rats: Involvement of nitric oxide-cyclic GMP-ATP sensitive K+ channels pathway and serotoninergic system

Antonio Espinosa de los Monteros-Zuñiga, Teresa Izquierdo, Geovanna Nallely Quiñonez-Bastidas, Héctor Isaac Rocha-González, Beatriz Godínez-Chaparro

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

© 2016 The neurobiology of neuropathic pain is caused by injury in the central or peripheral nervous system. Recent evidence points out that mangiferin shows anti-nociceptive effect in inflammatory pain. However, its role in inflammatory and neuropathic pain and the possible mechanisms of action are not yet established. The purpose of this study was to determine the possible anti-allodynic effect of mangiferin in rats with spinal nerve ligation (SNL). Furthermore, we sought to investigate the possible mechanisms of action that contribute to these effects. Mechanical allodynia to stimulation with the von Frey filaments was measured by the up and down method. Intrathecal administration of mangiferin prevented, in a dose-dependent fashion, SNL-induced mechanical allodynia. Mangiferin-induced anti-allodynia was prevented by the intrathecal administration of L-NAME (100 μg/rat, non-selective nitric oxide synthase inhibitor), ODQ (10 μg/rat, inhibitor of guanylate-cyclase) and glibenclamide (50 μg/rat, channel blocker of ATP-sensitive K+ channels). Moreover, methiothepin (30 μg/rat, non-selective 5-HT receptor antagonist), WAY-100635 (6 μg/rat, selective 5-HT1A receptor antagonist), SB-224289 (5 μg/rat, selective 5-HT1B receptor antagonist), BRL-15572 (4 μg/rat, selective 5-HT1D receptor antagonist) and SB-659551 (6 μg/rat, selective 5-HT5A receptor antagonist), but not naloxone (50 μg/rat, non-selective opioid receptor antagonist), were able to prevent mangiferin-induced anti-allodynic effect. These data suggest that the anti-allodynic effect induced by mangiferin is mediated at least in part by the serotoninergic system, involving the activation of 5-HT1A/1B/1D/5A receptors, as well as the nitric oxide-cyclic GMP-ATP-sensitive K+ channels pathway, but not by the opioidergic system, in the SNL model of neuropathic pain in rats.
Original languageAmerican English
Pages (from-to)190-197
Number of pages170
JournalPharmacology Biochemistry and Behavior
DOIs
StatePublished - 1 Nov 2016

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