The research of neuronal apoptosis and oxidative stress in the hippocampus of alcohol-associated dementia rat model

Objective To study the role of neuronal apoptosis and oxidative stress in the mechanism of the ethanolinduced damage of learning and memory function in alcohol-associated dementia( AAD) rat model. Methods SD rats were intragastricly administrated with ethanol( 20%,8ml / kg) for 28 days. Animals were evaluated by observing Morris Maze behavior and detecting the neuronal apoptosis in rat hippocampus. The activities of total superoxide dismutase( T-SOD) and glutathione peroxidase( GSH-Px) in rat blood serum were also measured. Results As compared to saline group( 4. 52 ± 1. 14,sec),the escape latency( EL) time of rat receiving ethanol was apparently extended( 9. 08 ± 1. 12,sec.)( P 0. 05), which suggests the learning and memory function of rats was damaged by ethanol administration. The number of apoptosis neuron was apparently increased in rat hippocampus after ethanol-intragastric administration. As compared to saline group, the activity of GSH-Px was significantly inhibited in the blood serum of rats treated with ethanol,but not for T-SOD. Conclusions The damage of learning and memory function induced by ethanol is closely related with its effects on the suppression of GSH-Px activity and the induction of neuron apoptosis in the hippocampus.