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


OBJECTIVE
This study evaluates the possible mechanism by which hydroalcoholic extract (HE) of Pfaffia glomerata exerts its antinociceptive effect.


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.


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.


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.
Department of Pharmacology, Sector of Biological Sciences, Federal University of Paraná, Curitiba, PR, Brazil.
Cristina Setim
CS
Freitas
Cristiane Hatsuko
CH
Baggio
André
A
Twardowschy
Ana Cristina
AC
dos Santos
Bárbara
B
Mayer
Ana Paula
AP
Luiz
Cid Aimbiré Moraes
CA
dos Santos
Maria Consuelo Andrade
MC
Marques
Adair Roberto Soares
AR
dos Santos
D019342:Acetic Acid; D027703:Amaranthaceae; D000700:Analgesics / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D003515:Cycloleucine; D004195:Disease Models, Animal; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology*; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism; D007278:Injections, Spinal; D053583:Interleukin-1beta; D051379:Mice; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D010146:Pain / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology* / Q000627:therapeutic use; D018517:Plant Roots; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D000700:Analgesics; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D053583:Interleukin-1beta; D009292:Narcotic Antagonists; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D003515:Cycloleucine; D009270:Naloxone; D018698:Glutamic Acid; D019342:Acetic Acid