Mori Fructus improves cognitive and neuronal dysfunction induced by beta-amyloid toxicity through the GSK-3β pathway in vitro and in vivo.

J Ethnopharmacol 2015 Aug 9;171:196-204. Epub 2015 Jun 9.

College of Pharmacy and Kyung Hee East-West Pharmaceutical Research Institute, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 130-701, Republic of Korea; Department of Life and Nanopharmaceutical Science, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 130-701, Republic of Korea. Electronic address:

Ethnopharmacological Relevance: A growing body of literature supports the concept that antiaging herbs may be potential candidates for use in treating age-related neurodegeneration, including Alzheimer׳s disease (AD). Mori Fructus is a well-known traditional herbal medicine, food, and dietary supplement. This study employed models of amyloid beta (Aβ)-induced AD to investigate the protective effects of Mori Fructus ethanol extract (ME) against age-related disease and cognitive deficits.

Materials And Methods: To examine the protective effect of ME, we measured cell viability, cytotoxicity, and survival in rat primary hippocampal cultures. We performed behavioral tests and histological analysis in mouse models of AD induced by Aβ(25-35) toxicity. To investigate the mechanism underlying the protective effect, we performed western blotting using antibodies against apoptotic markers as well as the nonphosphorylated and phosphorylated forms of Akt, glycogen synthase kinase-3β (GSK-3β), and tau. We also measured apoptotic marker fluorescence intensity.

Results: ME significantly attenuated Aβ-induced cell damage, enhanced Akt and GSK-3β phosphorylation, and reduced tau phosphorylation. ME reduced apoptotic markers that were activated by GSK-3β, and reduced reactive oxygen species production. Further, ME decreased the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X expression ratio, mitochondria depolarization, cytochrome c release from mitochondria, and caspase-3 activation. We confirmed that ME treatment improved cognitive impairment and neuronal cell death induced by Aβ(25-35) toxicity in the mouse hippocampus via its antiapoptotic activity.

Conclusions: These results indicate that ME protects cognition and neurons in AD-like models induced by Aβ via reduction of tau phosphorylation and apoptosis through GSK-3β inactivation.

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http://dx.doi.org/10.1016/j.jep.2015.05.054DOI Listing
August 2015
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