Salvianolic Acid B Inhibits A[beta] Generation by Modulating BACE1 Activity in SH-SY5Y-APPsw Cells

Alzheimer's disease (AD) is a neurodegenerative disease in humans. The accumulation of amyloid-[beta] (A[beta]) plays a critical role in the pathogenesis of AD. Previous studies indicated that Salvianolic acid B (SalB) could ameliorate A[beta]-induced memory impairment. However, whether SalB co...

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Bibliographic Details
Published in:Nutrients 2016-06, Vol.8 (6), p.333
Main Authors: Tang, Ying, Huang, Dan, Zhang, Mei-Hua, Zhang, Wen-Sheng, Tang, Yu-Xin, Shi, Zheng-Xiang, Deng, Li, Zhou, Dai-Han, Lu, Xin-Yi
Format: Article
Language:English
Subjects:
Alzheimer's disease
Biological products
Cosmetics
Herbal medicine
Hospitals
Kinases
Maternal & child health
Medicine
Oxidative stress
Pharmaceuticals
Proteins
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Summary:Alzheimer's disease (AD) is a neurodegenerative disease in humans. The accumulation of amyloid-[beta] (A[beta]) plays a critical role in the pathogenesis of AD. Previous studies indicated that Salvianolic acid B (SalB) could ameliorate A[beta]-induced memory impairment. However, whether SalB could influence the generation of A[beta] is unclear. Here, we show that SalB (25, 50, or 100 µM) reduces the generation of A[beta]40 and A[beta]42 in culture media by decreasing the protein expressions of BACE1 and sAPP[beta] in SH-SY5Y-APPsw cells. Meanwhile, SalB increases the levels of ADAM10 and sAPPα in the cells. However, SalB has no impact on the protein expressions of APP and PS1. Moreover, SalB attenuates oxidative stress and inhibits the activity of GSK3[beta], which might be related to the suppression of BACE1 expression and amyloidogenesis. Our study suggests that SalB is a promising therapeutic agent for AD by targeting A[beta] generation.
ISSN:2072-6643
DOI:10.3390/nu8060333