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...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 E_2(PGE_2) induced mechanical hyperalgesia and vincristine induced neuropathic pain in rat, both with analgesymeter. Modulators of NO/cG MP/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 PGE_2 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 antihyperalgesic effect could probably be associated with an activation of opioid receptors and NO/cG MP/K^+ channel pathway.展开更多
基金supported by the TWAS(Academy of Science of Developing Countries)International Center for Chemical and Biological SciencesUniversity of Karachi,under the Postdoctoral Fellowship Award to Mbiantcha Marius(RF N°:3240280477)
文摘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 E_2(PGE_2) induced mechanical hyperalgesia and vincristine induced neuropathic pain in rat, both with analgesymeter. Modulators of NO/cG MP/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 PGE_2 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 antihyperalgesic effect could probably be associated with an activation of opioid receptors and NO/cG MP/K^+ channel pathway.
