School of Chinese Medicine; Department of Chemistry; Department of Biology
Being one of the hallmarks of Alzheimer’s disease, β-amyloid (Aβ) aggregates induce complicated neurotoxicity. Evidences show that the underlying mechanism of neurotoxicity involves a glutamate receptor subtype, N-methyl-D-aspartate (NMDA) receptor, an increase in intracellular calcium(II) ion loading as well as an elevation in oxidation stress. In this work, among the 35 chemical components of Chinese herbal medicines (CHMs) being screened for inhibitors of Aβ aggregation, four of them, namely albiflorin, aloeemodin, neohesperidin and physcion, were found for the first time to exhibit a potent inhibitory effect on Aβ(1-40) and Aβ(1-42) aggregation. Their neuroprotective capability on primary hippocampal neuronal cells was also investigated by MTT assay, ROS assay and intracellular calcium(II) ion concentration measurement. It was interesting to find that physcion was rather toxic to neuronal cells while albiflorin, aloeemodin and neohesperidin reduced the toxicity and ROS induced by both monomeric and oligomeric Aβ species. In addition, albiflorin was particularly powerful in maintaining the intracellular Ca(2+) concentration.
Amyloid aggregation, calcium influx, herbs, inhibitors, neuroprotection, reactive oxygen species
Source Publication Title
Current Alzheimer Research
Bentham Science Publishers
The published manuscript is available at EurekaSelect via http://www.eurekaselect.com/openurl/content.php?genre=article&doi=10.2174/1567205012666150504144919
Link to Publisher's Edition
Ho, See-Lok, Chung-Yan Poon, Chengyuan Lin, Ting Yan, Wei Jing Daniel Kwong, Kin Lam Yung, Man Shing Ricky Wong, Zhaoxiang Bian, and Hung Wing Li. "Inhibition of β-amyloid aggregation by albiflorin, aloeemodin and neohesperidin and their neuroprotective effect on primary hippocampal cells against β-amyloid induced toxicity." Current Alzheimer Research 12.5 (2015): 424-433.