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  • PMID: 28447571 was deleted because it is a duplicate of PMID: 29390878
Cell Transplant. 2017 Dec;26(12):1903-1918. doi: 10.1177/0963689717738785.

Neuroprotective Effects of Betulin in Pharmacological and Transgenic Caenorhabditis elegans Models of Parkinson's Disease.

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1 Department of Nutrition, China Medical University, Taichung, Taiwan.
2 Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
3 Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
4 Translational Medicine Research Center, China Medical University Hospital, Taichung, Taiwan.
5 Department of Biochemical and Molecular Biology, National Cheng Kung University, Tainan, Taiwan.
6 Bioinnovation Center, Tzu Chi foundation, Department of Neurosurgery, Buddhist Tzu Chi General Hospital, Tzu Chi University, Hualien, Taiwan.
7 Department of Psychology, Asia University, Taichung, Taiwan.


Parkinson's disease (PD) is the second most common degenerative disorder of the central nervous system in the elderly. It is characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta, as well as by motor dysfunction. Although the causes of PD are not well understood, aggregation of α-synuclein (α-syn) in neurons contributes to this disease. Current therapeutics for PD provides satisfactory symptom relief but not a cure. Treatment strategies include attempts to identify new drugs that will prevent or arrest the progressive course of PD by correcting disease-specific pathogenic process. Betulin is derived from the bark of birch trees and possesses anticancer, antimicrobial, and anti-inflammatory properties. The aim of the present study was to evaluate the potential for betulin to ameliorate PD features in Caenorhabditis elegans ( C. elegans) models. We demonstrated that betulin diminished α-syn accumulation in the transgenic C. elegans model. Betulin also reduced 6-hydroxydopamine-induced dopaminergic neuron degeneration, reduced food-sensing behavioral abnormalities, and reversed life-span decreases in a pharmacological C. elegans model. Moreover, we found that the enhancement of proteasomes activity by promoting rpn1 expression and downregulation of the apoptosis pathway gene, egl-1, may be the molecular mechanism for betulin-mediated protection against PD pathology. Together, these findings support betulin as a possible treatment for PD and encourage further investigations of betulin as an antineurodegenerative agent.


Caenorhabditis elegans; Parkinson’s disease; betulin; dopaminergic neurons; neuroprotection; α-synuclein


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