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

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.