Effects induced by Apis mellifera venom and its components in experimental models of nociceptive and inflammatory pain

The effects induced by Apis mellifera venom (AMV), melittin-free AMV, fraction with molecular mass < 10 kDa (F<10) or melittin in nociceptive and inflammatory pain models in mice were investigated. Subcutaneous administration of AMV (2, 4 or 6 mg/kg) or melittin-free AMV (1, 2 or 4 mg/kg) into...

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Published in:Toxicon (Oxford) Vol. 57; no. 5; pp. 764 - 771
Main Authors: Merlo, Leonardo A., Bastos, Leandro F.S., Godin, Adriana M., Rocha, Leonardo T.S., Nascimento, Elias B., Paiva, André L.L., Moraes-Santos, Tasso, Zumpano, Antônio A.C., Bastos, Esther M.A.F., Heneine, Luiz Guilherme D., Coelho, Márcio M.
Format: Journal Article
Language:English
Published: Kidlington Elsevier Ltd 01-04-2011
Elsevier
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Summary:The effects induced by Apis mellifera venom (AMV), melittin-free AMV, fraction with molecular mass < 10 kDa (F<10) or melittin in nociceptive and inflammatory pain models in mice were investigated. Subcutaneous administration of AMV (2, 4 or 6 mg/kg) or melittin-free AMV (1, 2 or 4 mg/kg) into the dorsum of mice inhibited both phases of formaldehyde-induced nociception. However, F<10 (2, 4 or 6 mg/kg) or melittin (2 or 3 mg/kg) inhibited only the second phase. AMV (4 or 6 mg/kg), but not F<10, melittin-free AMV or melittin, induced antinociception in the hot-plate model. Paw injection of AMV (0.05 or 0.10 mg), F<10 (0.05 or 0.1 mg) or melittin (0.025 or 0.050 mg) induced a nociceptive response. In spite of inducing nociception after paw injection, scorpion (Tityus serrulatus) or snake (Bothrops jararaca) venom injected into the dorsum of mice did not inhibit formaldehyde-induced nociception. In addition, AMV (6 mg/kg), but not F<10 (6 mg/kg) or melittin (3 mg/kg), inhibited formaldehyde paw oedema. Concluding, AMV, F<10 and melittin induce two contrasting effects: nociception and antinociception. AMV antinociception involves the action of different components and does not result from non-specific activation of endogenous antinociceptive mechanisms activated by exposure to noxious stimuli.
Bibliography:http://dx.doi.org/10.1016/j.toxicon.2011.02.010
ObjectType-Article-1
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ISSN:0041-0101
1879-3150
DOI:10.1016/j.toxicon.2011.02.010