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目的探讨限食对D-半乳糖诱导的脑老化小鼠脑组织氧化损伤的保护作用。方法3月龄ICR小鼠40只分4组,即脑老化模型组、脑老化限食组、限食组和普通对照组。以D-半乳糖100mg/(kg·d)皮下注射法建立脑老化模型,限食鼠则按正常热能摄入量的70%投喂。实验干预9周后,先以Morris水迷宫实验测定小鼠空间学习记忆能力,再取大脑测定抗氧化酶SOD、GSH-Px活性及丙二醛(MDA)含量。结果①水迷宫实验:D-半乳糖脑老化小鼠逃避潜伏期明显大于对照小鼠(P<0.05),限食处理的脑老化小鼠逃避潜伏期显著低于脑老化鼠(P<0.05)而与正常对照组无显著差异。②生化检测:D-半乳糖脑老化小鼠脑内SOD、GSH-Px活性显著低于对照小鼠(P<0.05),限食脑老化小鼠脑内SOD、GSH-Px活性显著高于脑老化鼠(P<0.05)而与正常对照组无显著差异。但限食对正常小鼠脑组织SOD、GSH-Px活性未见显著影响。脑老化小鼠脑内MDA含量显著升高而限食可使MDA含量维持在接近正常对照组水平。结论在本试验条件下,限食能减轻脑老化小鼠认知功能衰退及脑组织抗超氧阴离子自由基酶活性下降,保护大脑免遭D-半乳糖氧化损伤所致脑老化。
Objective To investigate the protective effect of dietary restriction on oxidative damage in brain of aged mice induced by D-galactose. METHODS: Forty 4-month-old ICR mice were divided into 4 groups, namely brain aging model group, brain aging limited food group, restricted food group and normal control group. The brain aging model was established by subcutaneous injection of D-galactose 100mg/(kg·d). Rats were fed 70% of the normal caloric intake. After 9 weeks of experimental intervention, Morris water maze test was used to determine the spatial learning and memory ability of mice. The brains were then used to measure the activities of antioxidant enzymes SOD, GSH-Px and malondialdehyde (MDA) content. Results 1 Water maze test: The escape latency of D-galactose-induced brain aging mice was significantly greater than that of control mice (P<0.05). The escape latency of brain aging mice treated with food-resistance was significantly lower than that of brain aging mice (P<0.05). There was no significant difference in the normal control group. 2Biochemical assay: The activity of SOD and GSH-Px in the brain of D-galactose-induced brain aging mice was significantly lower than that of the control mice (P<0.05). The activities of SOD and GSH-Px in brains of rats with aging-enhanced brain were significantly higher than those in brains of aging rats. Aging mice (P<0.05) were not significantly different from normal controls. However, dietary restriction had no significant effect on the activity of SOD and GSH-Px in the brain of normal mice. The content of MDA in the brain of mice with aging brain increased significantly and the food restriction could maintain the content of MDA in the near normal control group. Conclusion Under the experimental conditions, diet restriction can reduce the decline of cognitive function in brain aging mice and the decrease of anti-superoxide anion free radical activity in brain tissue, and protect brain from brain aging caused by D-galactose oxidative injury.