Antipyretic and antinociceptive effects of Nauclea latifolia root decoction and possible mechanisms of action.

نویسندگان

  • Germain Sotoing Taïwe
  • Elisabeth Ngo Bum
  • Emmanuel Talla
  • Théophile Dimo
  • Norbert Weiss
  • Neteydji Sidiki
  • Amadou Dawe
  • Fleur Clarisse Okomolo Moto
  • Paul Désiré Dzeufiet
  • Michel De Waard
چکیده

CONTEXT  Nauclea latifolia Smith (Rubiaceae) is a small tree found in tropical areas in Africa. It is used in traditional medicine to treat malaria, epilepsy, anxiety, pain, fever, etc. OBJECTIVE  The aim of this study was to investigate the effects of Nauclea latifolia roots decoction on the peripheral and central nervous systems and its possible mechanisms of action. MATERIALS AND METHODS  The analgesic investigation was carried out against acetic acid-induced writhing, formalin-induced pain, hot-plate and tail immersion tests. The antipyretic activity was studied in Brewer's yeast-induced pyrexia in mice. Rota-rod test and bicuculline-induced hyperactivity were used for the assessment of locomotor activity. RESULTS  Nauclea latifolia induced hypothermia and had antipyretic effects in mice. The plant decoction produced significant antinociceptive activity in all analgesia animal models used. The antinociceptive effect exhibited by the decoction in the formalin test was reversed by the systemic administration of naloxone, N(ω)-L-nitro-arginine methyl ester or glibenclamide. In contrast, theophylline did not reverse this effect. Nauclea latifolia (antinociceptive doses) did not exhibit a significant effect on motor coordination of the mice in Rota-rod performance. Nauclea latifolia protected mice against bicuculline-induced behavioral excitation. DISCUSSION AND CONCLUSION  Overall, these results demonstrate that the central and peripheral effects of Nauclea latifolia root decoction might partially or wholly be due to the stimulation of peripheric opioid receptors through the action of the nitric oxide/cyclic monophosphate guanosin/triphosphate adenosine (NO/cGMP/ATP)-sensitive- K(+) channel pathway and/or facilitation of the GABAergic transmission.

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عنوان ژورنال:
  • Pharmaceutical biology

دوره 49 1  شماره 

صفحات  -

تاریخ انتشار 2011