Hibifolin, a flavonol glycoside, prevents β-amyloid-induced neurotoxicity in cultured cortical neurons

The toxicity of aggregated β-amyloid (Aβ) has been implicated as a critical cause in the development of Alzheimer's disease (AD). Hibifolin, a flavonol glycoside derived from herbal plants, possessed a strong protective activity against cell death induced by aggregated Aβ. Application of hibifolin in primary cortical neurons prevented the Aβ-induced cell death in a dose-dependent manner. In cultured cortical neurons, the pre-treatment of hibifolin abolished Aβ-induced Ca2+ mobilization, and also reduced Aβ-induced caspase-3 and caspase-7 activation. Moreover, DNA fragmentation induced by Aβ could be suppressed by hibifolin. In addition to such protection mechanisms, hibifolin was able to induce Akt phosphorylation in cortical neurons, which could be another explanation for the neuroprotection activity. These results therefore provided the first evidence that hibifolin protected neurons against Aβ-induced apoptosis and stimulated Akt activation, which would be useful in developing potential drugs or food supplements for treating AD.