Induction of autophagy by vasicinone protects neural cells from mitochondrial dysfunction and attenuates paraquat-mediated parkinson’s disease associated α-synuclein levels

Chih Yang Huang, Kalaiselvi Sivalingam, Marthandam Asokan Shibu, Po Hsiang Liao, Tsung Jung Ho, Wei Wen Kuo, Ray Jade Chen, Cecilia Hsuan Day, Vijaya Padma Viswanadha, Da Tong Ju

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

Abstract

Mitochondrial dysfunction and disturbed mitochondrial dynamics were found to be common phenomena in the pathogenesis of Parkinson’s disease (PD). Vasicinone is a quinazoline alkaloid from Adhatoda vasica. Here, we investigated the autophagy/mitophagy-enhancing effect of vasicinone and explored its neuroprotective mechanism in paraquat-mimic PD modal in SH-SY5Y cells. Vasicinone rescued the paraquat-induced loss of cell viability and mitochondrial membrane potential. Subsequently, the accumulation of mitochondrial reactive oxygen species (ROS) was balanced by an increase in the expression of antioxidant enzymes. Furthermore, vasicinone restored paraquat-impaired autophagy and mitophagy regulators DJ-1, PINK-1 and Parkin in SH-SY5Y cells. The vasicinone mediated autophagy pathways were abrogated by treatment with the autophagy inhibitor 3-MA, which lead to increases α-synuclein accumulation and decreased the expression of p-ULK and ATG proteins and the autophagy marker LC3-II compared to that observed without 3-MA treatment. These results demonstrated that vasicinone exerted neuroprotective effects by upregulating autophagy and PINK-1/Parkin mediated mitophagy in SH-SY5Y cells.

Original languageEnglish
Article number1707
Pages (from-to)1-16
Number of pages16
JournalNutrients
Volume12
Issue number6
DOIs
Publication statusPublished - Jun 2020

Keywords

  • Mitophagy
  • Paraquat
  • Parkinson’s disease
  • Reactive oxygen species
  • Vasicinone
  • α-synuclein

ASJC Scopus subject areas

  • Food Science
  • Nutrition and Dietetics

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