Bee venom and its component apamin as neuroprotective agents in a Parkinson disease mouse model

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Acupuncture Points
  • Animals
  • Apamin / pharmacology*
  • Bee Venoms / pharmacology*
  • Behavior, Animal / drug effects
  • Corpus Striatum / drug effects
  • Corpus Striatum / metabolism
  • Disease Models, Animal
  • Dopaminergic Neurons / drug effects*
  • Exploratory Behavior / drug effects
  • MPTP Poisoning / prevention & control
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neuroprotective Agents / pharmacology*
  • Parkinson Disease / prevention & control*
  • Tumor Necrosis Factor-alpha / metabolism


  • Bee Venoms
  • Neuroprotective Agents
  • Tumor Necrosis Factor-alpha
  • Apamin

Grant support

This study was funded by the Michael J. Fox Foundation. CN was supported by a postdoctoral grant from the Deutsche Forschungsgemeinschaft (DFG). DAF was funded by a grant from the University Medical Center Giessen and Marburg (UKGM). ECH is an investigator at the Centre National pour la Recherche Scientifique (CNRS). PPM and AH were supported by program “Investissements d'avenir” ANR-10-IAIHU-06. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.