摘要

Increased expression and aggregation of alpha-synuclein (alpha-syn) protein plays a critical role in mediating the toxic effects of a number of neurodegenerative substances including metals. Thus, knockdown expression of alpha-syn is proposed as a possible modality for treatment of Parkinson disease (PD). Aluminum (Al) is a neurotoxic metal that contributes to pathogenesis of PD. The aim of this study was to investigate the role of alpha-syn protein in mediating Al-induced toxicity in PC12 cells. Specific alpha-s3m small interference RNA (siRNA) was applied to knockdown the expression of alpha-syn protein in PC12 cells. The effects of different concentrations of Al-maltolate (Almal) were then evaluated on cell viability and oxidative stress in the alpha-syn downregulated cells. The results showed that Almal dose dependently induced apoptosis and increased malondialdehyde (MDA) and catalase activity in PC12 cells. Downregulation of alpha-syn protein significantly increased cell viability and decreased oxidative markers in Almal-treated cells. These findings suggest that alpha-syn protein may mediate Al-induced apoptosis and oxidative stress in PC12 cells.

  • 出版日期2016-3-15