Objective To establish an animal model of aging,to observe changes related to cognitive impairment and depression-like behavior,and to explore the mechanisms of the two diseases caused by the model.Methods Male Sprague-Dawley (SD) rats were treated with D-galactose and alchlor;after simultaneous administration of both drugs,their learning and memory abilities were assessed using the Morris water maze test.The depression-like behavioral changes were observed in the forced swimming test.Golgi staining was performed to observe the development of hippocampal neurons;oxidative stress index changes in superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were analyzed in the hippocampus.Results Compared with a control group,rats in the model group showed reduced escape latency (P ＜ 0.05) from the platform in the water maze,reduced residence time on and a reduced number of times passing through the platform (P ＜ 0.05);the real time in the water during the forced swimming test was significantly prolonged (P ＜ 0.01).Golgi staining indicated that dendritic spine density in the hippocampus in model rats was decreased (P ＜ 0.01),as was hippocampus SOD activity (P ＜ 0.05),while MDA levels were increased (P ＜ 0.05).Conclusion We established a new animal model of aging with cognitive impairment and depression.The common disease mechanisms of these two diseases might be related to the destruction of the nervous system during the process of overload caused by free radicals and the resulting metabolic imbalance.%目的 建立一种大鼠衰老模型,观察其认知障碍和抑郁样行为的变化,并初步探讨该模型引发的2种疾病的共病机制.方法 SD雄性大鼠经D-半乳糖和三氯化铝联合给药后,采用Morris水迷宫测定其学习记忆能力,采用强迫游泳实验检测抑郁样行为的改变,采用高尔基染色观察海马区神经元的发育情况,检测超氧化物歧化酶(SOD)和丙二醛(MDA)含量,并分析氧化应激指标的改变.结果 与对照组相比,模型组大鼠在水迷宫中逃避潜伏期延长(P＜0.05),平台停留时间和经过平台的次数减少(P＜0.05),强迫游泳实验中在水中的不动时间明显延长(P＜0.01),高尔基染色显示模型组大鼠海马区树突棘密度明显降低(P＜0.01),海马区SOD活力下降(P＜0.05),MDA含量增加(P＜0.05).结论 建立了一种新的并发认知障碍和抑郁的动物模型,这2种疾病的共病机制可能与自由基超载和代谢失衡过程中神经系统生长发育遭到破坏有关.
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