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Involvement of glutamate and cytokine pathways on antinociceptive effect of Pfaffia glomerata in mice.

Authors :
Freitas CS
Baggio CH
Twardowschy A
dos Santos AC
Mayer B
Luiz AP
dos Santos CA
Marques MC
dos Santos AR
Source :
Journal of ethnopharmacology [J Ethnopharmacol] 2009 Apr 21; Vol. 122 (3), pp. 468-72. Date of Electronic Publication: 2009 Feb 03.
Publication Year :
2009

Abstract

Ethnopharmacological Relevance: Pfaffia glomerata (Spreng) Pedersen (Amaranthaceae) is a medicinal plant known in Brazil as "Paratudo" and "Brazilian ginseng" and is commonly used as tonic, antidiabetic and to treat gastric disorders.<br />Aim of the Study: This study evaluates the possible mechanism by which hydroalcoholic extract (HE) of Pfaffia glomerata exerts its antinociceptive effect.<br />Materials and Methods: The HE was evaluated in acetic acid and glutamate models of pain or by biting behavior following intrathecal (i.t.) administration of agonists of excitatory aminoacids (EAA) receptors glutamate and pro-inflammatory cytokines, IL-1beta and TNF-alpha in mice.<br />Results: Oral administration of HE produced dose-dependent inhibition of acetic acid-induced visceral pain and glutamate-induced pain, with ID(50) of 64.6 (47.7-87.5)mg/kg and ID(50) of 370.8 (253.4-542.7)mg/kg, respectively. The HE (300 mg/kg, p.o.) antinociception, in the acetic acid test, was not affected by i.p. treatment of animals with naloxone. In addition, HE (300 mg/kg, p.o.) inhibited the pain-related behaviors induced by i.t. injection of trans-ACPD and TNF-alpha, but not by NMDA, AMPA, kainate or IL-1beta.<br />Conclusions: Our results suggest that inhibition of glutamatergic metabotropic receptors and TNF-alpha may account for the antinociceptive action reported for the HE in models of chemical pain used in this study.

Details

Language :
English
ISSN :
1872-7573
Volume :
122
Issue :
3
Database :
MEDLINE
Journal :
Journal of ethnopharmacology
Publication Type :
Academic Journal
Accession number :
19429314
Full Text :
https://doi.org/10.1016/j.jep.2009.01.033