Published in:
01-09-2016 | Original Research Paper
The leguminous lectin of Lonchocarpus araripensis promotes antinociception via mechanisms that include neuronal inhibition of Na+ currents
Authors:
Renata Morais Ferreira Amorim, Alana Freitas Pires, Tiago dos Santos-Nascimento, Benildo S. Cavada, Kyria Santiago do Nascimento, João Batista Cajazeiras, José Henrique Leal-Cardoso, Mário Rogério Lima Mota, Ana Maria S. Assreuy
Published in:
Inflammation Research
|
Issue 9/2016
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Abstract
Objective and design
Sodium channels are highly expressed in nociceptive sensory neurons during hypernociceptive conditions. Based on the presence of a glycosidic portion in the sodium channel β subunit associated to the antinociceptive effect of leguminous lectins via lectin domain, this study investigated the antinociceptive activity of the lectin isolated from Lonchocarpus araripensis seeds (LAL) in mice behavioral models and in NaV current in the nociceptor of rat dorsal root ganglion (DRG).
Material/methods
LAL antinociceptive activity and the participation of opioid system, lectin domain and sodium channels were evaluated in Swiss mice models of nociception (formalin, capsaicin, hot plate, tail flick, von Frey) and in primary cultures of Wistar rats neurons of DRG (patch clamp).
Results
LAL presented inhibitory effects in the nociception induced by chemical and mechanical, but not by thermal stimuli and reduced total Na+ current. LAL activity was inhibited by the lectin association with its binding sugar N-acethyl-glucosamine.
Conclusion
LAL inhibits peripheral hypernociception by mechanisms that involve the lectin domain, inflammatory mediators and Na+ channels. The innovative inhibitory action of leguminous lectins on NaV current brings new insights for the investigation of sodium channels role in nociception.