Baicalin prevents the production of hydrogen peroxide and oxidative stress induced by Aβ aggregation in SH-SY5Y cells

Alzheimer's disease (AD) is a common form of neurodegenerative disease. Mounting evidence suggests that metal ions play a key role in the aggregation of amyloid beta peptide (A beta), which acts as a factor or cofactor in the etiopathogenesis of AD. Therefore, inhibition of A beta aggregation emerges as a potential approach for the treatment of AD. We have found that baicalin can interact with copper directly and inhibits A beta 1 -42 aggregation. In addition, baicalin protects SH-SY5Y cells from oxidative injuries induced by A beta 1-42 aggregation through decreasing H2O2 production that is normally formed as a deleterious by-product of beta amyloid aggregation and the formation of plaques. Taken together, these data indicate that baicalin may be a potential agent to inhibit A beta aggregation and thereby delay, mitigate or modify the progression of neurodegenerative diseases such as AD. Crown Copyright (C) 2011 Published by Elsevier Ireland Ltd. All rights reserved.