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BASIC RESEARCH
Year : 2018  |  Volume : 8  |  Issue : 3  |  Page : 150-159

NO-cGMP-K channel-dependent anti-nociceptive activities of methanol stem bark extract of Piptadeniastrum africanum (Mimosaceae) on rats


1 Laboratory of Animal Physiology and Phytopharmacology, Faculty of Science, University of Dschang, P.O. Box 67, Dschang, Cameroon
2 Dr. Panjwani Center for Molecular Medicine and Drug Research, International Center for Chemical and Biological Sciences, University of Karachi, Karachi 75270, Pakistan
3 H.E.J. Research Institute of Chemistry, International Center for Chemical and Biological Sciences, University of Karachi, Karachi 75270, Pakistan

Correspondence Address:
Mbiantcha Marius
Laboratory of Animal Physiology and Phytopharmacology, Faculty of Science, University of Dschang, P.O. Box 67, Dschang
Cameroon
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2221-1691.227996

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Objective: To explore anti-hyperalgesic properties of methanol extract of Piptadeniastrum africanum stem bark (PAME) and it possible action mechanism. Methods: PAME was tested on carrageenan induced hyperalgesia using plantar test (thermal) and analgesymeter (mechanical) in rats, on prostaglandin E2 (PGE2) induced mechanical hyperalgesia and vincristine induced neuropathic pain in rat, both with analgesymeter. Modulators of NO/ cGMP/K+ channel pathway and endogenous opioids receptor antagonists and/or agonists were used to determine the possible action mechanism of PAME. Results: PAME significantly decreased carrageenan induced thermal and mechanical hyperalgesia, as well as PGE2 induced mechanical hyperalgesia. PAME significantly protected the animals against the installation of neuropathic pain. Anti-nociception activity produced by PAME was significantly blocked in animals pre treated with all the antagonists (naloxone, NW-nitro-L-arginine methyl ester (L-NAME), methylene blue and glibenclamide). Conclusions: Results of this study reveal that, PAME administrate orally, can induce anti-hyperalgesic action against installation of inflammatory pain as well as neuropathic pain. The mechanism underlying PAME anti-hyperalgesic effect could probably be associated with an activation of opioid receptors and NO/cGMP/K+ channel pathway.


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