Comparison of the Protective Effects of Bee Venom Extracts with Varying PLA2 Compositions in a Mouse Model of Parkinson's Disease.

Kyung Kim,Se Kim,Minhwan Kim,Jaehwan Lee,Hat Jeon,Hyunsu Bae

doi:10.3390/toxins11060358

Abstract

Bee venom contains a number of pharmacologically active components, including enzymes and polypeptides such as phospholipase A2 (PLA2) and melittin, which have been shown to exhibit therapeutic benefits, mainly via attenuation of inflammation, neurotoxicity, and nociception. The individual components of bee venom may manifest distinct biological actions and therapeutic potential. In this study, the potential mechanisms of action of PLA2 and melittin, among different compounds purified from honey bee venom, were evaluated against Parkinson’s disease (PD). Notably, bee venom PLA2 (bvPLA2), but not melittin, exhibited neuroprotective activity against PD in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. MPTP-induced behavioral deficits were also abolished after bvPLA2 treatment, depending on the PLA2 content. Further, bvPLA2 administration activated regulatory T cells (Tregs) while inhibiting inflammatory T helper (Th) 1 and Th17 cells in the MPTP mouse model of PD. These results indicate that bvPLA2, but not melittin, protected against MPTP and alleviated inflammation in PD. Thus, bvPLA2 is a promising and effective therapeutic agent in Parkinson’s disease.

Highlights

Parkinson’s disease (PD) is an age-related neurodegenerative disorder characterized by the progressive loss of dopaminergic (DA) neurons in the substantia nigra [1]
Recent studies support the role of regulatory T cells (Tregs) in inhibiting T cell inflammatory factors associated with immunosuppressive activity in the brain, which is the potential target in neurodegenerative disease
2, and not compared with control mice. These findings suggest that bee venom PLA2 (bvPLA2), and not melittin, stimulated the and their immunosuppressive and anti-inflammatory activity

Summary

Introduction

Parkinson’s disease (PD) is an age-related neurodegenerative disorder characterized by the progressive loss of dopaminergic (DA) neurons in the substantia nigra [1]. Most cases of PD are of unclear etiology and occur sporadically. Evidence suggests that inflammation is one of the key contributing factors to the pathogenesis of PD [2]. The enhanced inflammatory response in PD has been detected in the post-mortem brain tissue of PD patients, which demonstrated increased. Numerous studies have expanded our understanding of the potential role of inflammation in PD pathogenesis. Recent studies support the role of regulatory T cells (Tregs) in inhibiting T cell inflammatory factors associated with immunosuppressive activity in the brain, which is the potential target in neurodegenerative disease

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Conclusion