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Hibifolin, a Flavonol Glycoside, Prevents Beta-Amyloid-Induced Neurotoxicity in Cultured Cortical Neurons

Hibifolin, a Flavonol Glycoside, Prevents Beta-Amyloid-Induced Neurotoxicity in Cultured Cortical Neurons

Judy T T Zhu, Roy C Y Choi, Heidi Q Xie, Ken Y Z Zheng, Ava J Y Guo, Cathy W C Bi, David T W Lau, Jun Li, Tina T X Dong, Brad W C Lau, Ji J Chen, Karl W K Tsim

Neurosci Lett. 2009 Sep 18;461(2):172-6.

PMID: 19539722

Abstract:

The toxicity of aggregated beta-amyloid (A beta) 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 A beta. Application of hibifolin in primary cortical neurons prevented the A beta-induced cell death in a dose-dependent manner. In cultured cortical neurons, the pre-treatment of hibifolin abolished A beta-induced Ca(2+) mobilization, and also reduced A beta-induced caspase-3 and caspase-7 activation. Moreover, DNA fragmentation induced by A beta 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 A beta-induced apoptosis and stimulated Akt activation, which would be useful in developing potential drugs or food supplements for treating AD.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP55366568	Hibifolin		55366-56-8	Price

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