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

• Published in: Neuroscience letters 2011-04, Vol.492 (2), p.76-79
• Main Authors: Yin, Fei, Liu, Jianhui, Ji, Xiuhong, Wang, Yanwen, Zidichouski, Jeffrey, Zhang, Junzeng
• Format: Article
• Language: English
• Subjects: Aggregation; Amyloid beta-Peptides - metabolism; Amyloid beta-Peptides - pharmacology; Amyloid beta-Peptides - ultrastructure; Antioxidants - pharmacology; Baicalin; Biological and medical sciences; Cell Line, Tumor; Copper; Copper - metabolism; Dose-Response Relationship, Drug; Drug Interactions; Flavanones - pharmacology; Fundamental and applied biological sciences. Psychology; Humans; Hydrogen peroxide; Hydrogen Peroxide - metabolism; Neuroblastoma - pathology; Oxidative Stress - drug effects; Peptide Fragments - metabolism; Peptide Fragments - pharmacology; Peptide Fragments - ultrastructure; Phenol - pharmacology; Plant Extracts - pharmacology; Scutellaria baicalensis; Time Factors; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2011.01.055

► Baicalin is a flavonoid compound from Chinese herb Huang Qin ( Scutellaria lateriflora Georgi). ► Baicalin interacts with copper, inhibits Aβ1–42 aggregation and reduces production of H 2O 2. ► Baicalin protects SH-SY5Y cells from Aβ1–42 induced oxidative stress. 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 2O 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.