Anti-Parkinsonian effects of beta-amyrin are regulated via LGG-1 involved autophagy pathway in Caenorhabditis elegans

作者：Wei Chia Cheng; Chang Chun Han; Liao Vivian Hsiu Chuan^*

来源：Phytomedicine, 2017, 36: 118-125.

DOI：10.1016/j.phymed.2017.09.002

• Anti-Parkinsonian effects
• beta-amyrin
• Caenorhabditis elegans
• Antioxidant
• alpha-synuclein
• LGG-1
• Autophagy

Background: Parkinson's disease (PD) is a neurodegenerative disease that is associated with aging and is characterized as a movement disorder. Currently, there is still no complete therapy for PD. In recent years, the identification and characterization of medicinal plants to cure or treat PD has gained increasing scientific interest.
Purpose: In this study, we investigated a pentacyclic triterpenoid compound, beta-amyrin, which is found in many medicinal plants for its anti-Parkinsonian effects, using Caenorhabditis elegans (C. elegans) disease models and their underlying mechanisms.
Methods: C. elegans treated or untreated with beta-amyrin were investigated for oxidative stress resistance, neurodegeneration, and alpha-synuclein aggregation assays. The C. elegans ortholog of Atg8/ LC3, LGG-1 that is involved in the autophagy pathway was also evaluated by quantitative RT-PCR and transgenic strain experiments.
Results: beta-Amyrin exerted excellent antioxidant activity and reduced intracellular oxygen species in C. elegans. Using the transgenic strain BZ555, beta-amyrin showed a protective effect on dopaminergic neurons reducing cell damage induced by 6-hydroxydopamine (6-OHDA). In addition, beta-amyrin significantly reduced the a-synuclein aggregation in the transgenic strain NL5901. Moreover, beta-amyrin up-regulated LGG-1 mRNA expression and increased the number of localized LGG-1 puncta in the transgenic strain DA2123.
Conclusion: The results from this study suggest that the anti-Parkinsonian effects of beta-amyrin might be regulated via LGG-1 involved autophagy pathway in C. elegans. Therefore, beta-amyrin may be useful for therapeutic applications or supplements to treat or slow the progression of PD.

• 出版日期2017-12-1