Neuroprotective effects of Eucommia ulmoides Oliv. Bark on amyloid beta(25-35)-induced learning and memory impairments in mice
- Authors
- Kwon, Seung-Hwan; Lee, Ha-Kyung; Kim, Ji-Ah; Hong, Sa-Ik; Kim, Sun-Yeou; Jo, Tae-Hyung; Park, Young-In; Lee, Chong-Kil; Kim, Yong-Bin; Lee, Seok-Yong; Jang, Choon-Gon
- Issue Date
- 3-1월-2011
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Eucommia ulmoides Oliv. Bark; Amyloid beta(25-35); Acetylcholinerase; Alzheimer' s disease
- Citation
- NEUROSCIENCE LETTERS, v.487, no.1, pp.123 - 127
- Indexed
- SCIE
SCOPUS
- Journal Title
- NEUROSCIENCE LETTERS
- Volume
- 487
- Number
- 1
- Start Page
- 123
- End Page
- 127
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/113292
- DOI
- 10.1016/j.neulet.2010.10.042
- ISSN
- 0304-3940
- Abstract
- In the present study, we examined whether aqueous extract of Eucommia ulmoides Oliv. Bark (EUE) with graded doses exerted its neuroprotective effects on amyloid beta(25-35) (A beta(25-35))-induced learning and memory impairments in mice. Mice received a single intracerebroventricular (i.c.v.) injection of A beta(25-35) 6 nmol as the critical factor in Alzheimer's disease (AD), cognition was evaluated using Y-maze, passive avoidance, and Morris water maze tests. EUE significantly improved the A beta(25-35)-induced memory deficit in the Y-maze test. Also, EUE increased step-through latency time with A beta(25-35)-induced learning and memory deficits in the passive avoidance test. In addition, EUE decreased the escape latencies with A beta(25-35)-induced cognitive impairments in the Morris water maze test. In the probe trial session. EUE increased time spent in the target quadrant. In the in vitro study, EUE was found to inhibit acetylcholinesterase (AChE) activity in a dose-dependent manner (IC50 value; 172 mu g/ml). Ex vivo study. EUE significantly inhibited AChE activity in the hippocampus and frontal cortex. These results demonstrate that EUE possesses potent neuroprotective effects and that its beneficial effects are mediated, in part, by AChE inhibition, and therefore, might be a potential candidate in neurodegenerative diseases such as AD. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
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