Neuroprotective effects of Eucommia ulmoides Oliv. Bark on amyloid beta25–35-induced learning and memory impairments in mice

In the present study, we examined whether aqueous extract of Eucommia ulmoides Oliv. Bark (EUE) with graded doses exerted its neuroprotective effects on amyloid beta25–35 (Aβ25–35)-induced learning and memory impairments in mice. Mice received a single intracerebroventricular (i.c.v.) injection of Aβ25–35 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 Aβ25–35-induced memory deficit in the Y-maze test. Also, EUE increased step-through latency time with Aβ25–35-induced learning and memory deficits in the passive avoidance test. In addition, EUE decreased the escape latencies with Aβ25–35-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.

Research highlights▶ EUE may improve short-term and working memory by rescuing cholinergic synaptic function. ▶ EUE has neuroprotective effects on long-term memory impairment induced by Aβ25–35 treatment. ▶ Ameliorative effect of EUE on long-term and reference memory impairment due to rescuing the acetylcholine system from deficits by Aβ25–35 treatment. ▶ EUE improves learning and memory deficits in Aβ25-35-treated mouse models via blocking AChE activity.