Departamento de Produtos Farmacêuticos, Universidade Federal de Minas Gerais, Avenida Antônio Carlos 6627, 31270-901 Belo Horizonte, MG, Brazil.
Toxicon. 2011 Apr;57(5):764-71. doi: 10.1016/j.toxicon.2011.02.010. Epub 2011 Feb 17.
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.
研究了蜜蜂毒液 (AMV)、无蜂毒素 AMV、<10 kDa 分子量的馏分 (F<₁₀) 或蜂毒素在小鼠疼痛和炎症模型中的作用。将 AMV(2、4 或 6 mg/kg)或无蜂毒素 AMV(1、2 或 4 mg/kg)皮下注射到小鼠背部,可抑制甲醛诱导的疼痛的两个阶段。然而,F<₁₀(2、4 或 6 mg/kg)或蜂毒素(2 或 3 mg/kg)仅抑制第二阶段。AMV(4 或 6 mg/kg)而非 F<₁₀、无蜂毒素 AMV 或蜂毒素在热板模型中引起镇痛作用。AMV(0.05 或 0.10 mg)、F<₁₀(0.05 或 0.1 mg)或蜂毒素(0.025 或 0.050 mg)注射到爪子会引起疼痛反应。尽管爪子注射后会引起疼痛,但蝎子(Tityus serrulatus)或蛇(Bothrops jararaca)毒液注射到小鼠背部不会抑制甲醛诱导的疼痛。此外,AMV(6 mg/kg)而非 F<₁₀(6 mg/kg)或蜂毒素(3 mg/kg)抑制甲醛引起的爪子水肿。结论是,AMV、F<₁₀ 和蜂毒素引起两种相反的作用:疼痛和镇痛。AMV 的镇痛作用涉及不同成分的作用,而不是由暴露于伤害性刺激激活的内源性镇痛机制的非特异性激活引起的。