Cyanidin 3-O-glucopyranoside protects and rescues SH-SY5Y cells against amyloid-beta peptide-induced toxicity.

The amyloid-beta (A beta) peptide (1-42) aggregation into oligomeric and fibrillar species affects neuronal viability, having a causal role in the development of Alzheimer's disease. Among dietary anthocyanins, cyanidin 3-O-glucoside (Cy-3G) and its metabolites, such as protocatechuic acid (PA), have gained attention as potential neuroprotective agents. In this in-vitro study, we demonstrated that Cy-3G, but not PA, can inhibit A beta1-42 spontaneous aggregation using thioflavin T fluorescence assay and transmission electron microscopy. Furthermore, treatment of human neuronal SH-SY5Y cells with Cy-3G during oligomeric and fibrillar A beta1-42 treatment prevents neuronal viability loss. These protective effects were still evident when Cy-3G treatment was initiated after the appearance of oligomeric A beta1-42 neurotoxicity. Taken together, these results suggest that Cy-3G may protect and rescue the neuronal cells from toxicity induced by A beta1-42.