Comparison of Administration Routes on the Protective Effects of Bee Venom Phospholipase A2 in a Mouse Model of Parkinson’s Disease

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.

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Bee Venom Phospholipase A2, a Novel Foxp3+Regulatory T Cell Inducer, Protects Dopaminergic Neurons by Modulating Neuroinflammatory Responses in a Mouse Model of Parkinson’s Disease

The Journal of Immunology ◽

10.4049/jimmunol.1500386 ◽

2015 ◽

Vol 195 (10) ◽

pp. 4853-4860 ◽

Cited By ~ 39

Author(s):

Eun Sook Chung ◽

Gihyun Lee ◽

Chanju Lee ◽

Minsook Ye ◽

Hwan-suck Chung ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

T Cell ◽

Mouse Model ◽

Phospholipase A2 ◽

Regulatory T Cell ◽

Dopaminergic Neurons ◽

Bee Venom

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Neuro-protective effects of bee venom by suppression of neuroinflammatory responses in a mouse model of Parkinson’s disease: Role of regulatory T cells

Brain Behavior and Immunity ◽

10.1016/j.bbi.2012.08.013 ◽

2012 ◽

Vol 26 (8) ◽

pp. 1322-1330 ◽

Cited By ~ 40

Author(s):

Eun Sook Chung ◽

Himchan Kim ◽

Gihyun Lee ◽

Soojin Park ◽

Hyunseong Kim ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

T Cells ◽

Regulatory T Cells ◽

Mouse Model ◽

Bee Venom ◽

Protective Effects

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Neuroprotective Effects of a GLP-2 Analogue in the MPTP Parkinson’s Disease Mouse Model

Journal of Parkinson s Disease ◽

10.3233/jpd-202318 ◽

2021 ◽

pp. 1-15

Author(s):

Zijuan Zhang ◽

Li Hao ◽

Ming Shi ◽

Ziyang Yu ◽

Simai Shao ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Substantia Nigra ◽

Mouse Model ◽

Neurodegenerative Disorder ◽

Enzyme Linked Immunosorbent Assay ◽

Protective Effects ◽

Neuroprotective Effects ◽

Expression Levels ◽

Dual Agonist

Background: Glucagon-like peptide 2 (GLP-2) is a peptide hormone derived from the proglucagon gene expressed in the intestines, pancreas and brain. Some previous studies showed that GLP-2 improved aging and Alzheimer’s disease related memory impairments. Parkinson’s disease (PD) is a progressive neurodegenerative disorder, and to date, there is no particular medicine reversed PD symptoms effectively. Objective: The aim of this study was to evaluate neuroprotective effects of a GLP-2 analogue in the 1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) PD mouse model. Methods: In the present study, the protease resistant Gly(2)-GLP-2 (50 nmol/kg ip.) analogue has been tested for 14 days by behavioral assessment, transmission electron microscope, immunofluorescence histochemistry, enzyme-linked immunosorbent assay and western blot in an acute PD mouse model induced by MPTP. For comparison, the incretin receptor dual agonist DA5-CH was tested in a separate group. Results: The GLP-2 analogue treatment improved the locomotor and exploratory activity of mice, and improved bradykinesia and movement imbalance of mice. Gly(2)-GLP-2 treatment also protected dopaminergic neurons and restored tyrosine hydroxylase expression levels in the substantia nigra. Gly(2)-GLP-2 furthermore reduced the inflammation response as seen in lower microglia activation, and decreased NLRP3 and interleukin-1β pro-inflammatory cytokine expression levels. In addition, the GLP-2 analogue improved MPTP-induced mitochondrial dysfunction in the substantia nigra. The protective effects were comparable to those of the dual agonist DA5-CH. Conclusion: The present results demonstrate that Gly(2)-GLP-2 can attenuate NLRP3 inflammasome-mediated inflammation and mitochondrial damage in the substantia nigra induced by MPTP, and Gly(2)-GLP-2 shows neuroprotective effects in this PD animal model.

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