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Int J Mol Sci. 2018 Feb 17;19(2). pii: E598. doi: 10.3390/ijms19020598.

The Cyanthin Diterpenoid and Sesterterpene Constituents of Hericium erinaceus Mycelium Ameliorate Alzheimer's Disease-Related Pathologies in APP/PS1 Transgenic Mice.

Author information

1
Institute of Biopharmaceutical Science, National Yang-Ming University, Taipei 112, Taiwan. fly23242530@hotmail.com.
2
Department of Cosmetic Science, Chang Gung University of Science and Technology, Kweishan, Taoyuan 333, Taiwan. chen37426972@gmail.com.
3
Biotechnology Center, Grape King Bio Ltd. Chung-Li, Taoyuan 320, Taiwan. gkbioeng@grapeking.com.tw.
4
Institute of Neuroscience, Brain Research Center, School of Life Science, National Yang-Ming University, Taipei 112, Taiwan. hjtsay@ym.edu.tw.
5
Biotechnology Center, Grape King Bio Ltd. Chung-Li, Taoyuan 320, Taiwan. ly.lee@grapeking.com.tw.
6
Biotechnology Center, Grape King Bio Ltd. Chung-Li, Taoyuan 320, Taiwan. hjtsay@ym.edu.tw.
7
National Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei 112, Taiwan. wp.chen@grapeking.com.tw.
8
Institute of Biopharmaceutical Science, National Yang-Ming University, Taipei 112, Taiwan. yshiao@nricm.edu.tw.
9
National Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei 112, Taiwan. yshiao@nricm.edu.tw.

Abstract

Hericium erinaceus was used in traditional Chinese medicine for physiologically beneficial medicines. Recently, it has become a candidate in causing positive brain health-related activities. We previously reported that Hericium erinaceus mycelium ameliorates Alzheimer's disease (AD)-related pathologies. To reveal the role of the cyanthin diterpenoid and sesterterpene constituents on this effects, erinacine A and S were isolated and their effects on attenuating AD-related pathology in APPswe/PS1dE9 transgenic mice were investigated. A 30 day short-term administration of erinacine A and S were performed to explore the effect of each erinacine on AD-related pathology including amyloid β production and degradation, plaque formation, plaque growth, glial activation and neurogenesis deterioration. Our results indicated the benefit effects of both erinacine A and S in cerebrum of APPswe/PS1dE9 mice, including: (1) attenuating cerebral plaque loading by inhibiting plaque growth; (2) diminishing the activation of glial cells; (3) raising the level of insulin degrading enzyme; and (4) promoting hippocampal neurogenesis. Moreover, erinacine A reduced the level of insoluble amyloid β and C-terminal fragment of amyloid precursor protein which was not mediated by erinacine S. We further performed a long term administration of erinacine A and found that erinacine A recovered the impairment in the tasks including burrowing, nesting, and Morris water maze. Our data pointed out that although both erinacine A and S reduce AD pathology via reducing amyloid deposition and promoting neurogenesis, erinacine A can also inhibit amyloid β production and is worth to be further developed for AD therapeutic use.

KEYWORDS:

APPswe/PS1dE9 transgenic mice; Alzheimer’s disease; amyloid plaque; astrocytes; erinacines; microglia; neurogenesis

PMID:
29463001
PMCID:
PMC5855820
DOI:
10.3390/ijms19020598
[Indexed for MEDLINE]
Free PMC Article

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