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 β peptide (Aβ), which acts as a factor or cofactor in the etiopathogenesis of AD. Therefore, inhibition of Aβ aggregation emerges as a potential approach for the treatment of AD. We have found that baicalin can interact with copper directly and inhibits Aβ1-42 aggregation. In addition, baicalin protects SH-SY5Y cells from oxidative injuries induced by Aβ1-42 aggregation through decreasing H(2)O(2) 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 Aβ aggregation and thereby delay, mitigate or modify the progression of neurodegenerative diseases such as AD.