Protective effect of edaravone against Aβ25-35-induced mitochondrial oxidative damage in SH-SY5Y cells

G. L. Zhang, L. Zhang, Y. Y. Guo, Z. L. Ma, H. Y. Wang, T. Li, J. Liu, Y. Du, L. Yao, T. T. Li, J. M. Du

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Amyloid-β (Aβ)-induced oxidative stress plays an important role in the pathogenesis of Alzheimer's disease (AD). Recent studies show that Aβ accumulation may lead to mitochondrial oxidative damage. In the present study, we investigated the protective effect of edaravone on mitochondrial damage in SH-SY5Y cells treated with Aβ25-35. SH-SY5Y cells were pre-treated with 20, 40 or 80 μM edaravone before treatment with 25 μM Aβ25-35. After 24h cell culture, cellular apoptosis, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨm), ATP levels and mitochondrial morphology were evaluated. SH-SY5Y cells exposed to Aβ25-35 had high levels of apoptosis and ROS; loss of ΔΨm, decreased ATP levels and presence of mitochondrial swelling. However, these effects were significantly inhibited by edaravone pre-treatment. These results indicate that edaravone prevents mitochondria oxidative damage caused by Aβ in SH-SY5Y cells, which suggests that it may have potential clinical application in AD therapy.

Original languageEnglish (US)
Article number8
Pages (from-to)36-42
Number of pages7
JournalCellular and Molecular Biology
Issue number5
StatePublished - 2017
Externally publishedYes


  • Alzheimer's disease
  • Amyloid-β peptide
  • Edaravone
  • Mitochondria damage

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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