Journal
PHARMACOLOGICAL REPORTS
Volume 69, Issue 6, Pages 1341-1348Publisher
POLISH ACAD SCIENCES INST PHARMACOLOGY
DOI: 10.1016/j.pharep.2017.06.006
Keywords
Tau hyperphosphorylation; Cognitive dysfunction; Oxidative stress; Inflammation; Berberine
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Funding
- Chongqing General Hospital [CGHK201701]
- Natural Science Foundation of Hubei Province [2015CFB260]
- Hubei Province Health and Family Planning Scientific Research Project [WJ2015MB219]
- Shiyan Natural Science Foundation [15K70]
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Background: Berberine (BBR) plays an important role in the prevention and treatment of Alzheimer's disease (AD). The present work was to explore whether BBR ameliorates cognitive deficits in AD and to investigate whether its underlying mechanism involves inhibiting hyperphosphorylated tau protein. Methods: The cognitive function was measured by the Morris water maze (MWM) test. The levels of hyperphosphorylated tau proteins were determined by Western blot. The biomarkers of NF-kappa B signaling pathway and oxidative stress were detected by Western blot and biochemical assays. The biomarkers of neuroinflammation were determined by Western blot and immunohistochemistry. Results: BBR improved learning and memory in APP/PS1 mice. BBR decreased the hyperphosphorylated tau protein in the hippocampus of APP/PS1 mice. BBR lowered the activity of NF-kB signaling in the hippocampus of AD mice. BBR-administration promoted the activity of glutathione (GSH) and inhibited lipid peroxidation in the hippocampus of AD mice. Conclusion: BBR attenuated cognitive deficits and limited hyperphosphorylation of tau via inhibiting the activation of NF-kB signaling pathway, and by retarding oxidative stress and neuro-inflammation. (c) 2017 Published by Elsevier Sp. z o.o. on behalf of Institute of Pharmacology, Polish Academy of Sciences.
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