Neuroprotective effect of magnolol in the hippocampus of senescence-accelerated mice (SAMP1)

We investigated age-dependent neuronal loss in the hippocampus and the protective effect of magnolol using SAMP1 mice in comparison with SAMR1. SAMP1 and SAMR1, 2 to 10 months old, were used. Magnolol (2 and 5 mg/kg) was orally administered once a day for 7 days to 2-month-old mice and evaluation was carried out at 4 months. The density of neurofibrils and axons decreased with aging in the CA1 and CA3 regions of the hippocampus. The rate of decrease in SAMP1 was greater than that of SAMR1. Treatment with magnolol dose-dependently prevented the decrease of density in CA1 and CA3 at 4 months. However, until the age of 4 months, SAMP1 animals did not behaviorally differ from SAMR1 either with or without magnolol. It has been suggested that imbalance between the rates of generation and utilization of reactive oxygen species (ROS) and organic free radicals may be one of the main reasons for accelerated aging of SAMP1 animals. These findings suggest that the antioxidant and free radical scavenging activity of magnolol may contribute to the protective effect against neuronal loss in the hippocampus. (C) 2003 Elsevier B.V All rights reserved.