TLR4/NF-κB-IN-2

ICR mice (male, 6-8 weeks old, 18-25 g, intracerebroventricular injection of Aβ_1-42 peptide-induced)^[1]

2.5 mg/kg; 10 mg/kg

p.o.; once daily for 7 consecutive days

Reversed Aβ_1-42-induced reductions in total ambulatory distance, mean speed, and central zone movement distance in the open-field test.
Reduced escape latency over 5 days of Morris water maze training, increased the number of platform crossings, and increased time spent in the target quadrant during the probe trial.
Reduced hippocampal Aβ_1-42 concentrations from ~70 μg/L to ~60 μg/L (2.5 mg/kg) and to ~48 μg/L (10 mg/kg); reduced whole-brain Aβ_1-42 concentrations from ~42 μg/L to ~38 μg/L (2.5 mg/kg) and to ~31 μg/L (10 mg/kg).
Increased neuronal counts in the DG, CA1, and CA3 regions of the hippocampus; at 10 mg/kg, increased DG neuronal counts from ~240 to ~460 and CA1 neuronal counts from ~80 to ~150.
Dose-dependently reduced the percentage of GFAP-positive astrocytes and Iba-1-positive microglia in the hippocampus, shifting glial cells from a reactive to a resting morphological state.
Reduced hippocampal TNF-α levels from ~185 pg/mL to ~148 pg/mL (2.5 mg/kg) and to ~105 pg/mL (10 mg/kg); reduced IL-6 levels from ~228 pg/mL to ~165 pg/mL (2.5 mg/kg) and to ~135 pg/mL (10 mg/kg).
Reduced hippocampal MDA levels from ~180 nmol/mgprot to ~165 nmol/mgprot (2.5 mg/kg) and to ~120 nmol/mgprot (10 mg/kg); increased SOD activity from ~2.8 U/mgprot to ~3.8 U/mgprot (2.5 mg/kg) and to ~4.2 U/mgprot (10 mg/kg).