Université Pierre et Marie Curie-Paris 6, UMR_S 975 - UMR 7725, Centre de Recherche en Neurosciences, ICM, Therapeutique Experimentale de la Neurodegenerescence, Paris, France.
PLoS One. 2013 Apr 18;8(4):e61700. doi: 10.1371/journal.pone.0061700. Print 2013.
Bee venom has recently been suggested to possess beneficial effects in the treatment of Parkinson disease (PD). For instance, it has been observed that bilateral acupoint stimulation of lower hind limbs with bee venom was protective in the acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. In particular, a specific component of bee venom, apamin, has previously been shown to have protective effects on dopaminergic neurons in vitro. However, no information regarding a potential protective action of apamin in animal models of PD is available to date. The specific goals of the present study were to (i) establish that the protective effect of bee venom for dopaminergic neurons is not restricted to acupoint stimulation, but can also be observed using a more conventional mode of administration and to (ii) demonstrate that apamin can mimic the protective effects of a bee venom treatment on dopaminergic neurons. Using the chronic mouse model of MPTP/probenecid, we show that bee venom provides sustained protection in an animal model that mimics the chronic degenerative process of PD. Apamin, however, reproduced these protective effects only partially, suggesting that other components of bee venom enhance the protective action of the peptide.
蜂毒最近被认为在治疗帕金森病 (PD) 方面具有有益的效果。例如，已经观察到，用蜂毒对下肢双侧穴位刺激对 PD 的急性 1-甲基-4-苯基-1,2,3,6-四氢吡啶 (MPTP) 小鼠模型具有保护作用。特别是，蜂毒的一种特定成分，蜂毒肽，以前被证明对体外多巴胺能神经元具有保护作用。然而，迄今为止，尚无关于蜂毒肽在 PD 动物模型中潜在保护作用的信息。本研究的具体目标是 (i) 确定蜂毒对多巴胺能神经元的保护作用不仅限于穴位刺激，而且还可以使用更常规的给药方式观察到，以及 (ii) 证明蜂毒肽可以模拟蜂毒治疗对多巴胺能神经元的保护作用。使用慢性 MPTP/丙磺舒小鼠模型，我们表明蜂毒在模拟 PD 慢性退行性过程的动物模型中提供持续的保护。然而，蜂毒肽仅部分重现了这些保护作用，表明蜂毒的其他成分增强了肽的保护作用。
