Protective effect of erythropoietin on β-amyloid-induced PC12 cell death through antioxidant mechanisms

Erythropoietin (EPO), a haematopoietic growth factor has been reported to display neuroprotective properties in different animal models. In the present study, we investigated the neuroprotective effects of EPO on Aβ25-35-induced neuronal toxicity and its potential mechanisms in PC12 cells. Aβ25-35 significantly reduced cell viability and increased the number of apoptotic-like cells. In addition, increased ROS production and decreased mitochondrial membrane potential were also found after Aβ25-35 exposure. All of these phenotypes induced by Aβ25-35 were markedly reversed by EPO. Pretreatment with EPO prior to Aβ25-35 exposure significantly elevated cell viability, reduced Aβ25-35-induced apoptosis, decreased ROS production, and stabilized mitochondrial membrane potential. Furthermore, EPO also attenuated the downstream cascade following ROS, including Bcl-2/Bax, and caspase-3 activation. Our results suggest that EPO holds potential for neuroprotection and therefore, may be promising for the treatment of Alzheimer's disease.