Bee Venom and Its Component Apamin As Neuroprotective Agents in a Parkinson Disease Mouse Model

Overview

Journal PLoS One

Specialties General Medicine
Science

Date 2013 May 3

PMID 23637888

Citations 53

Authors

Daniel Alvarez-Fischer

Carmen Noelker

Franca Vulinovic

Anne Grunewald

Caroline Chevarin

Christine Klein

Wolfgang H Oertel

Etienne C Hirsch

Patrick P Michel

Andreas Hartmann

Affiliations

Soon will be listed here.

Abstract

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.

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