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.
Highlights
IntroductionParkinson disease (PD) is a neurodegenerative disorder characterized by typical motor symptoms (akinesia, rigidity, rest tremor) that result from the progressive loss of dopamine (DA) neurons in the substantia nigra (SN) [1]
Parkinson disease (PD) is a neurodegenerative disorder characterized by typical motor symptoms that result from the progressive loss of dopamine (DA) neurons in the substantia nigra (SN) [1]
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 [3][4]
Summary
Parkinson disease (PD) is a neurodegenerative disorder characterized by typical motor symptoms (akinesia, rigidity, rest tremor) that result from the progressive loss of dopamine (DA) neurons in the substantia nigra (SN) [1]. 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 [3][4]. This observation is of interest in view of possible pharmacological interventions aimed at modifying disease progression. The molecular target of this effect requires to be characterized since bee venom is composed of many chemical agents including polypeptides, enzymes and amines [5] It remains to be established whether the protective effect of bee venom is specific to administration through acupoint stimulation
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