Antinociceptive activities of the methanol extract of the bulbs of Dioscorea bulbifera L. var sativa in mice is dependent of NO-cGMP-ATP-sensitive-K(+) channel activation

Télesphore B Nguelefack, Rafael C Dutra, Ana F Paszcuk, Edinéia L Andrade, Léon A Tapondjou, João B Calixto
Journal of Ethnopharmacology 2010 April 21, 128 (3): 567-74

ETHNOPHARMACOLOGICAL RELEVANCE: Dioscorea bulbifera var sativa is a medicinal plant commonly used in Cameroonian traditional medicine to treat pain and inflammation.

AIM: The present work evaluated the effects of the methanol extract of the bulbs of Dioscorea bulbifera in inflammatory and neuropathic models of pain and further investigated its possible mechanism of action.

MATERIALS AND METHODS: The effects of Dioscorea bulbifera administered orally at the doses of 250 and 500mg/kg were tested in mechanical hypernociception induced by intraplantar ( injection of complete Freund's adjuvant (CFA), lipopolysaccharides (LPS) or prostaglandin-E(2) (PGE(2)), as well as in partial ligation sciatic nerve (PLSN), nociception induced by capsaicin and thermal hyperalgesia induced by injection of CFA. The therapeutic effects of Dioscorea bulbifera on PGE(2)-induced hyperalgesia were evaluated in the absence and in the presence of l-NAME, an inhibitor of nitric oxide synthase (NOS) and glibenclamide, an inhibitor of ATP-sensitive potassium channels.

RESULTS: The extract showed significant antinociceptive effects in persistent pain induced by CFA and on neuropathic pain induced by PLSN. The effects of Dioscorea bulbifera persisted for 5 days after two administrations in CFA-induced hypernociception. Dioscorea bulbifera significantly inhibited acute LPS-induced pain but failed to reduce thermal hypernociception and capsaicin-induced spontaneous nociception. The antinociceptive effects of this plant extract in PGE(2) model was antagonized by either l-NAME or glibenclamide.

CONCLUSION: Present demonstrate the antinociceptive activities of Dioscorea bulbifera both in inflammatory and neuropathic models of pain and these effects may result, at least partially, from its ability to activate the NO-cGMP-ATP-sensitive potassium channels pathway.

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