Protective effect of Cy-3G on PC12 cells against beta-amyloid-induced apoptosis and the possible mechanism

Beta-amyloid protein (Abeta), a major protein component of brain senile plaques in Alzheimer’s disease, is known to be directly responsible for the production of reactive oxygen species (ROS) and induction of apoptosis. In this study, the protective effect of cyanidin 3-O-glucopyranoside (Cy-3G), an anthocyanin derivate purified from fruits, on Abeta-induced rat pheochromocytoma (PC12) cultures was investigated. Although exposure of PC12 cells to 50 μM Abeta25-35 caused significant viability loss and apoptotic rate increase, pretreatment of the cells with Cy-3G for 2 h reduced the viability loss and apoptotic rate. Cy-3G (20 μM) significantly inhibited Abeta25-35-induced apoptosis of PC12 cells. Preincubation of the cell with Cy-3G also restored the ROS and mitochondrial membrane potential levels that had been altered as a result of Abeta25-35 treatment. Cy-3G was also found to excite the Cyt c and AIF release to cytoplasm and reduce caspase-3, caspase-8 and caspase-9 activation. Phosphorylation of JNK and P38 were also suppressed by Cy-3G. These results suggested that Cy-3G could attenuate Abeta25-35-induced PC12 cell injury and apoptosis through regulating JNK and P38 MAPK signaling. Therefore, Cy-3G may act as an intracellular ROS scavenger, and its antioxidant properties may protect against Abeta25-35-induced cell injury.