酒精性痴呆大鼠海马神经细胞凋亡与氧化应激的研究

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

目的探讨酒精诱导学习记忆功能损害与海马神经细胞凋亡及氧化应激的关系。方法以SD大鼠为实验对象,给予持续28d酒精灌胃(20%,8ml/kg)建立酒精性痴呆大鼠模型,观察大鼠Morris水迷宫行为和海马神经细胞凋亡状况,同时采用比色法检测大鼠血清总超氧化物歧化酶(T-SOD)和谷胱甘肽过氧化物酶(GSH-Px)的变化。结果与生理盐水组(4.52±1.14s)相比,酒精组大鼠的逃避潜伏期时间明显延长(9.08±1.12s)(P<0.05),且其海马区凋亡神经细胞数量明显增加(P<0.01)。氧化应激检测证实与生理盐水组相比,酒精组大鼠血清GSH-Px活性显著抑制(P<0.01),但T-SOD活性改变不明显。结论慢性酒精中毒可导致大鼠学习记忆功能损害,其机制与酒精诱导海马神经细胞凋亡及抑制抗氧化酶活性有关。

Objective To study the role of neuronal apoptosis and oxidative stress in the mechanism of the ethanol- induced 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 be- havior 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. Con- clusions The damage of learning and memory function induced by ethanol is closely related with its effects on the suppres- sion of GSH-Px activity and the induction of neuron apoptosis in the hippocampus.