Protective effects of Glycyrrhiza uralensis Fisch. on the cognitive deficits caused by β-amyloid peptide 25–35 in young mice

Abstract

Amyloid beta protein (Abeta) may be involved in the progression of Alzheimer's disease (AD), by acting as a neurotoxin and eliciting oxidative stress. This study was designed to determine the effects of Glycyrrhiza uralensis Fisch. water extract (GWE) on the cognitive deficits and oxidative stress induced by the administration of Abeta(25-35) in mice. Mice in two of the four animal groups were fed an experimental diet containing either 0.5 or 1% GWE for the entire 6-week experimental period. Control mice and a further experimental group were fed a non-GWE diet. Abeta(25-35) was administered to the three experimental groups by intracerebroventricular (i.c.v.) injection (10 microg/10 microl/mouse) once per week in weeks 5 and 6 of the experimental period. Behavioral changes were assessed using both a passive avoidance (after the injection of Abeta(25-35) in week 5) and the Morris water-maze tests (after the injection of Abeta(25-35) in week 6). Control animals were administered vehicle alone. The prolonged consumption of a diet containing GWE ameliorated the cognitive deficits caused by the i.c.v. injections of Abeta(25-35). Treatment with Abeta(25-35) led to higher concentrations of thiobarbituric acid reactive substances in the brain, and GWE attenuated this response. There was a decrease in catalase activity in the group provided with 1% GWE. Acetylcholinesterase activity was significantly reduced in the brains of all GWE-treated animals compared to that in the non-GWE-fed experimental group. These results suggest that GWE exerts a protective effect against the cognitive impairments often observed in AD, and that in mice this effect is mediated by antioxidant actions against oxidative stress.

Sesaminol Glucosides Protect .BETA.-Amyloid Peptide-Induced Cognitive Deficits in Mice

“…Ab [25][26][27][28][29][30][31][32][33][34][35] (Sigma-Aldrich Co., CA, U.S.A.) was dissolved in phosphate-buffered saline (PBS) and injected into animals at the beginning of each behavioral test trial by i.c.v. (10 mg/10 ml/mouse) according to the procedure established by Lauren and Belknap.…”

“…Passive Avoidance Test The day before Ab [25][26][27][28][29][30][31][32][33][34][35] injection (at beginning of 5 weeks), mice were trained on a passive avoidance task. Passive avoidance was tested using a two-compartment shuttle chamber (256000 series, TSE Systems, Germany), one illuminated and one dark, equipped with a grid floor and shock generator.…”

“…During the training trial, each mouse was placed in the lit compartment, and as soon as it entered the dark compartment, the door was closed and it received an inescapable shock (0.3 mA, 3 s). The day after Ab [25][26][27][28][29][30][31][32][33][34][35] injection, the mouse was again placed in the lit compartment, and the time until it returned to the dark compartment was measured as the step-through latency (with a maximum of 300 s). If the mouse did not enter the dark compartment within 300 s, the mouse was assumed to have memorized the passive avoidance training after one training trial.…”

“…When a mouse located the platform, it was permitted to remain on it for 10 s. If the mouse did not locate the platform within 120 s, it was placed on the platform for 10 s. In each training trial, the time required to find the hidden platform was recorded. After several trials, the probe trial was conducted after the second injection of Ab [25][26][27][28][29][30][31][32][33][34][35] (at beginning of 6 weeks).…”

“…But, no significant difference between the two groups was observed (data not shown). Considering this fact, we performed experiments with Ab [25][26][27][28][29][30][31][32][33][34][35] .…”