Neuroprotective effects of Eucommia ulmoides Oliv. Bark on amyloid beta25–35-induced learning and memory impairments in mice
Male
Memory Disorders
Mice, Inbred ICR
0303 health sciences
Amyloid beta-Peptides
Dose-Response Relationship, Drug
Eucommiaceae
Hippocampus
Peptide Fragments
Frontal Lobe
3. Good health
Disease Models, Animal
Mice
03 medical and health sciences
Acetylcholinesterase
Plant Bark
Reaction Time
Animals
Plant Preparations
Maze Learning
Swimming
Phytotherapy
DOI:
10.1016/j.neulet.2010.10.042
Publication Date:
2010-10-26T08:46:36Z
AUTHORS (11)
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) (Aβ(25-35))-induced learning and memory impairments in mice. Mice received a single intracerebroventricular (i.c.v.) injection of Aβ(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 Aβ(25-35)-induced memory deficit in the Y-maze test. Also, EUE increased step-through latency time with Aβ(25-35)-induced learning and memory deficits in the passive avoidance test. In addition, EUE decreased the escape latencies with Aβ(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 μg/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.
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