自主性运动对β淀粉样蛋白_(25-35)诱导小鼠神经细胞凋亡及氧化应激水平的影响

Voluntary Exercise Influencing Neuron Apoptosis and Oxidative Stress in Aβ_(25-35) Mice

目的研究自主性运动对β淀粉样蛋白25-35(Aβ25-35)诱导小鼠学习记忆损伤的影响及其血清氧化应激水平的调控作用。方法采用2月龄C57bl/6雄性小鼠双侧侧脑室注射Aβ25-35快速部分模拟散发性阿尔茨海默病(AD)的学习记忆损伤;Y迷宫检测小鼠短期学习记忆能力;化学比色法检测血清丙二醛(MDA)、羟自由基、总抗氧化能力(T-AOC)、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)及总超氧化物歧化酶(T-SOD)活力;Hochest染色观察海马CA1区神经细胞损伤情况。结果与对照组相比,模型组短期学习记忆能力明显下降(进臂正确率:52.43±2.34、62.43±0.53,t=4.166,P=0.044);海马CA1区神经细胞凋亡比例明显增加(4.43±0.30、1.81±0.33,t=-5.863,P=0.004);血清MDA含量上升(43.51±5.22、21.03±1.29,t=-4.181,P=0.043)。与模型组相比较,治疗组小鼠短期学习记忆能力显著改善(进臂正确率:72.72±1.71,52.43±2.34,t=-6.838,P=0.002);海马CA1区神经细胞凋亡比例明显下降(2.86±0.22、4.43±0.30、t=4.260,P=0.013);血清GSH、GSH-Px、T-AOC活力显著提升。结论自主性运动能提高Aβ25-35小鼠抗氧化应激能力,减轻神经细胞损伤,改善Aβ25-35诱导的小鼠学习记忆缺陷。

Aim To investigate the influence of voluntary exercise on the impairment of memory and its effect on the regulation of serum levels of oxidative stress.Methods Intracerebroventricular injection of β-amyloid25-35（Aβ25-35） in two-month-old male C57bl/6 mice caused the impairment of learning and memory.After exercise training intervention,Y-maze was arranged to measure the short-term change of learning and memory.The levels of serum malondialdehyde（MDA）,hydroxy radical,total antioxidant capacity（T-AOC）,glutathione peroxidase（GSH-Px）,glutathione（GSH） and total superoxide dismutase（T-SOD） were quantitatively determined with methods of chemical colorimetry.Neuronal damage in the hippocampal CA1 region was observed by Hochest staining.Results Compared with the control group,the mice in the model group exhibited decreased learning and memory capacity（Alternation： 52.43±2.34,62.43±0.53,t=4.166,P=0.044） accompanied with elevated neuron apoptosis rate（4.43±0.30,1.81±0.33,t=-5.863,P=0.004） in the hippocampal CA1 region,and increased level of serum MDA（43.51±5.22,21.03±1.29,t=-4.181,P=0.043）.Compared with the model group,mice in the treatment group exhibited improved learning and memory capacity（Alternation： 72.72±1.71,52.43±2.34,t=-6.838,P=0.002）,decreased neuron apoptosis rate（2.86±0.22,4.43±0.30,t=4.260,P=0.013） in the hippocampal CA1 region and elevated vitality of T-AOC,GSH-Px and GSH.Conclusion Voluntary exercise may improve the ability of antioxidative stress in Aβ25-35 mice,alleviate hippocampal neuron apoptosis,and furthermore ameliorate learning and memory deficit induced by Aβ25-35.