Affiliations: [a] Department of Pathophysiology, Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China | [b] Wuhan Mental Health Center, Wuhan, China
Correspondence:
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Correspondence to: Xiaochuan Wang, Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Tel.: +86 27 83692 625; Fax: +86 27 83693883; Email: [email protected].
Note: [1] These authors contributed equally to the paper.
Abstract: The Chinese herb berberine has versatile health effects. Recent reports indicate that berberine has the potential to prevent and treat Alzheimer's disease (AD). In the present study, we employed tau-expressing HEK293 cells (HEK293/tau) treated with calyculin-A as a cellular model to investigate the roles of berberine in cell viability, tau phosphorylation, and oxidative stress. We found a significant reduction of calyculin A-induced tau hyperphosphorylation at Ser198/199/202, Ser396, Ser404, Thr205, and Thr231 24 h after treatment with 20 μg/ml berberine. Berberine also restored protein phosphates 2A activity and reversed glycogen synthase kinase-3β (GSK-3β) activation, as determined by phosphatase activity assay and GSK-3β phosphorylation at Tyr216 and Ser9, respectively. Furthermore, berberine reversed both the increase of malondialdehyde and the decrease of superoxide dismutase activity induced by calyculin A, indicating its role in anti-oxidative stress. Our findings suggest that berberine may be a potential therapeutic drug for AD.
Keywords: Alzheimer's disease, berberine, GSK-3β, PP2A, tau hyperphosphorylation
