Protective Effect of Edaravone Against AÎ²25-35-Induced Mitochondrial Oxidative Damage in SH-SY5Y Cells
Corresponding Author(s) : G-L. Zhang
Cellular and Molecular Biology,
Vol. 63 No. 5: Issue 5
Amyloid-Î² (AÎ²)-induced oxidative stress plays an important role in the pathogenesis of Alzheimer's disease (AD). Recent studies show that AÎ² 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 AÎ²25-35. SH-SY5Y cells were pre-treated with 20, 40 or 80 Î¼M edaravone before treatment with 25 Î¼M AÎ²25-35. After 24h cell culture, cellular apoptosis, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (Î”Î¨m), ATP levels and mitochondrial morphology were evaluated. SH-SY5Y cells exposed to AÎ²25-35 had high levels of apoptosis and ROS; loss of Î”Î¨m, 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 AÎ² in SH-SY5Y cells, which suggests that it may have potential clinical application in AD therapy.
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