February 1 2017
This substance is found in many herbs including abelmoschus manihot.
Hibifolin, a flavonol glycoside, prevents beta-amyloid-induced
neurotoxicity in cultured cortical neurons.
Neurosci Lett. 2009; Department of Biology and Center for Chinese Medicine, The Hong Kong University of Science and Technology, Clear Water Bay Road, Kowloon, Hong Kong SAR, China.
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.
Metabolism of Hibifolin by Human Intestinal Bacteria
Planta Med. 2009. Department of Natural Medicines and State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical , Sciences, Peking University Health Science Center, Beijing, P. R. China.
Hibifolin, the highest-content bioactive flavonoid of the flowers of Abelmoschus manihot, was incubated with human intestinal bacteria, and four metabolites The structures of the four metabolites were elucidated as gossypetin 8- O- beta- D-4''-deoxy- Delta(4'')-glucuropyranoside, gossypetin, quercetin, and 8-methoxy-quercetin.