Effect of Purple Sweet Potato Anthocyanins on β-Amyloid-Mediated PC-12 Cells Death by Inhibition of Oxidative Stress
Amyloid-beta peptide (Aβ) is known to induce the redox imbalance, mitochondrial dysfunction and caspase activation, resulting in neuronal cell death. Treatment with antioxidants provided a new therapeutic strategy for Alzheimer’s disease (AD) patients. Here we investigate the effects of purple sweet potato anthocyanins (PSPA), the known strong free radical scavengers, on Aβ toxicity in PC12 cells. The results showed that pretreatment of PC12 cells with PSPA reduced Aβ-induced toxicity, intracellular reactive oxygen species (ROS) generation and lipid peroxidation dose-dependently. In parallel, cell apoptosis triggered by Aβ characterized with the DNA fragmentation and caspase-3 activity were also inhibited by PSPA. The concentration of intracellular Ca2+ and membrane potential loss associated with cell apoptosis were attenuated by PSPA. These results suggested that PSPA could protect the PC-12 cell from Aβ-induced injury through the inhibition of oxidative damage, intracellular calcium influx, mitochondria dysfunction and ultimately inhibition of cell apoptosis. The present study indicates that PSPA may be a promising approach for the treatment of AD and other oxidative-stress-related neurodegenerative diseases.
KeywordsPSPA Amyloid β peptide (Aβ) Oxidative stress Reactive oxygen species (ROS) Apoptosis PC12 cells
Purple sweet potato anthocyanins
Reactive oxygen species
Relative fluorescence unit
Changes in intracellular free calcium levels
This work was supported by a grant from the Science and Technology Bureau of Qingdao (No. 03-2-JZ-03) and the Science Foundation of Shandong Provincial Educational Department, China (Grant No. J04E17).
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