Edaravone ameliorates oxidative damage associated with Aβ25-35 treatment in PC12 cells.

Oxidative damage is an important mediator of Alzheimer's disease (AD); hence, antioxidant therapy is a potential treatment for AD. Edaravone, a free radical scavenger, has been shown to have neuroprotective properties. The study aimed to examine the effects of edaravone on indicators of Aβ25-35-induced oxidative damage in PC12 cells. PC12 cells were treated with 20, 40, or 80 μM edaravone before treatment with 30 μM Aβ25-35. After treatment, the following assessments were performed: cell viability and aggregation, oxidative stress, mitochondrial peroxidation, generation of reactive oxygen species (ROS), and apoptosis. Aggregation, lactate dehydrogenase activity, malondialdehyde concentrations, mitochondrial peroxidation, ROS levels, and apoptosis were significantly increased in Aβ25-35-treated cells but decreased in the treatment with edaravone 40 and 80 μM. In contrast, intracellular glutathione and superoxide dismutase concentrations were significantly decreased in Aβ25-35-treated cells but increased in the treatment with edaravone 40 and 80 μM. Edaravone ameliorates oxidative damage associated with Aβ25-35 treatment in PC12 cells. Our findings support the continued investigation of edaravone as a potential treatment for AD.