β-Amyrin Ameliorates Alzheimer’s Disease-Like Aberrant Synaptic Plasticity in the Mouse Hippocampus
Hye Jin Park1,†, Huiyoung Kwon1,†, Ji Hye Lee2,†, Eunbi Cho1, Young Choon Lee1,3, Minho Moon4, Mira Jun3,5, Dong Hyun Kim1,3,* and Ji Wook Jung6,*
1Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, Busan 49315,
2Division of Endocrinology, School of Medicine, Kyungpook National University, Daegu 41944,
3Institute of Convergence Bio-Health, Dong-A University, Busan 49315,
4Department of Biochemistry, College of Medicine, Konyang University, Daejeon 35365,
5Department of Food Science and Nutrition, College of Health Sciences, Dong-A University, Busan 49315,
6Department of Herbal Medicinal Pharmacology, College of Herbal Bio-industry, Daegu Haany University, Kyungsan 38610, Republic of Korea
*E-mail: mose79@dau.ac.kr (Kim DH), jwjung@dhu.ac.kr (Jung JW)
Tel: +82-51-200-7583 (Kim DH), +82-53-819-1337 (Jung JW)
Fax: +82-51-200-5748 (Kim DH), +82-53-819-1338 (Jung JW)

The first three authors contributed equally to this work.
Received: February 8, 2019; Revised: June 13, 2019; Accepted: June 17, 2019; Published online: July 30, 2019.
© The Korean Society of Applied Pharmacology. All rights reserved.

Abstract
Alzheimer’s disease (AD) is a progressive and most frequently diagnosed neurodegenerative disorder. However, there is still no drug preventing the progress of this disorder. β-Amyrin, an ingredient of the surface wax of tomato fruit and dandelion coffee, is previously reported to ameliorate memory impairment induced by cholinergic dysfunction. Therefore, we tested whether β-amyrin can prevent AD-like pathology. β-Amyrin blocked amyloid β (Aβ)-induced long-term potentiation (LTP) impairment in the hippocampal slices. Moreover, β-amyrin improved Aβ-induced suppression of phosphatidylinositol-3-kinase (PI3K)/Akt signaling. LY294002, a PI3K inhibitor, blocked the effect of β-amyrin on Aβ-induced LTP impairment. In in vivo experiments, we observed that β-amyrin ameliorated object recognition memory deficit in Aβ-injected AD mice model. Moreover, neurogenesis impairments induced by Aβ was improved by β-amyrin treatment. Taken together, β-amyrin might be a good candidate of treatment or supplement for AD patients.
Keywords: β-amyrin, Amyloid β, Alzheimer’s disease, Synaptic plasticity


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