Vinpocetine attenuates the metabolic dysfunction induced by amyloid β-peptides in PC12 cells

The cytoprotective effect of vinpocetine [14-ethoxycarbonyl-(3 alpha ,16 alpha -ethyl)-14,15-eburnamine] was investigated on PC12 cells treated with the amyloid beta -peptides (A beta) for 24 hours. Vinpocetine was shown to protect cells from the inhibition in redox status induced by exposure to A beta (25-35) and A beta (1-40), the maximal protection being achieved at a vinpocetine concentration of 40 muM. At this concentration, vinpocetine blocked the inhibition of the mitochondrial respiratory chain complexes II-III and IV and completely abolished the depletion of pyruvate levels induced by toxic concentrations of A beta peptides. Furthermore, the accumulation of ROS in cells exposed to A beta (25-35) and A beta (1-40)evaluated using the fluorescent probe 2',7'-dichlorofluorescin (DCF), was reduced in the presence of 40 muM vinpocetine. Taken together, the data presented herein demonstrate that vinpocetine protects cells from A beta toxicity, preventing the generation of oxidative stress due to the excessive accumulation of ROS. This study suggests that vinpocetine can exert neuroprotective properties which might be of importance and contribute to its clinical efficacy in the treatment of Alzheimer's disease or other neurodegenerative disorders in which oxidative stress is involved.