有氧运动对老年大鼠海马氧化应激水平、AMPK及PGC-1α蛋白表达的影响

Research on the Mechanism of Long-term Aerobic Exercise Reducing Oxidative Stress in the Hippocampus of Aging Rats

目的初步探讨长期有氧运动改善老年大鼠海马氧化应激水平的机制。方法 16只24月龄雄性Wistar大鼠随机分对照组(CG)及运动组(EG),每组8只。EG组大鼠采用递增负荷跑台运动方案进行为期8周的有氧运动训练。最后一次训练结束24 h后,将所有大鼠断头取脑,分离两侧海马。分别采用化学荧光等方法对大鼠海马活性氧自由基(reactive oxygen species,ROS)、超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GPx)、脂质过氧化产物(丙二醛,malondialdehyde,MDA)进行检测,采用免疫印迹对海马ROS新陈代谢重要调解因子—过氧化物酶体增殖活化受体γ辅助活化因子1α(Peroxisome proliferator-activated receptor gamma coactivator 1-alpha,PGC-1α)及调解PGC-1α磷酸化的AMP激活蛋白激酶(AMP-activated protein kinase,AMPK)进行检测。结果本研究结果发现,与对照组相比,EG组大鼠海马ROS及MDA含量明显减少(P<0.05),SOD及GPx活性显著增加(P<0.05),PGC-1α及AMPK表达明显增强(P<0.05)。结论有氧运动可以有效地调节海马氧化还原平衡状态,延缓氧化应激引起的神经变性进程。AMPK的激活,PGC-1α蛋白表达的增加,可能是有氧运动改善海马氧化还原平衡状态的分子途径。

Objective To reveal the mechanism of long-term aerobic exercise reducing oxidative stress in the hippocampus of aging rats. Methods Sixteen 24-month old Wistar rats were randomly divided into control group（ CG） and exercise group（ EG）,each group consists of 8. Rats of EG group performed 8 weeks aerobic exercise with a gradually increased load treadmill exercise protocol. 24 hours after the last exercise,all rats were killed and hippocampus tissue was isolated. By using chemiluminescence and other methods,the reactive oxygen species（ ROS）,superoxide dismutase（ SOD）,glutathione peroxidase（ GPx） and malondialdehyde（ MDA） were detected. In addition,the peroxisome proliferator-activated receptor gamma coactivator 1-alpha（ PGC-1α） and AMP-activated protein kinase（ AMPK） in the hippocampus were detected as well through western blotting technique. Results The results showed that,compared with CG group,the ROS and MDA concentrations in rat hippocampus of EG group reduced significantly（ P 0. 05）,while,the SOD and GPx activity increased significantly（ P 0. 05）. A clear increase of PGC-1α and AMPK impression in EG group were seen as well. Conclusions Long-term physical exercise can comprises antioxidant properties and by this way protect neurons against oxidative stress-induced neural degeneration process. The up-regulation of AMPK and PGC-1α may partly account for the beneficial effects of exercise in the hippocampus.