中文摘要：

目的 肥胖是认知缺陷的独立危险因素,但相关机制仍待阐明.本研究旨在探讨有氧间歇训练（AIT）对高脂（HF）饮食诱导的肥胖小鼠海马神经元损伤的影响和可能的机制.方法 40只2个月龄C57小鼠随机分为：正常饮食对照组（Con）;正常饮食间歇训练组（Con＋ AIT）;高脂饮食组（HF）;高脂饮食间歇训练组（HF＋ AIT）.部分实验中采用20只2月龄去乙酰化酶3（SIRT3）敲除小鼠（KO）随机分为：高脂敲除组（HF KO）;高脂敲除间歇训练组（HF KO＋ AIT）.12 w后测定各组小鼠学习记忆能力,海马神经元的氧化应激程度及凋亡.结果 与正常饮食对照组相比,12 w HF喂养导致小鼠肥胖,体重显著增加.Morris水迷宫定位航行实验显示,高脂饮食（HF）小鼠逃避潜伏期显著延长;平台搜索实验中,HF小鼠在目标象限的停留时间显著缩短（P＜0.05）.HF组海马神经元丙二醛（MDA）和活性氧（ROS）水平显著升高,而海马神经元线粒体抗氧化酶：锰超氧化物歧化酶（MnSOD）和过氧化氢酶（catalase）的活性却显著降低（均P＜0.05）.并且,HF组海马神经元中SIRT3表达水平显著减少.与HF组相比,AIT可显著增强HF小鼠海马神经元SIRT 3表达进而增强其下游MnSOD和Catalase活性,减少HF组海马神经元氧化应激,并改善学习记忆能力.但是,在SIRT 3敲除小鼠中,AIT对HF小鼠海马神经元的保护作用在被显著抑制（均P＜0.05）.结论 AIT可有效上调海马神经元SIRT 3表达,增加线粒体抗氧化酶活性,进而改善HF小鼠认知能力.SIRT 3可能是AIT抑制HF海马神经元损伤的关键因子.

英文摘要：

Objective Obesity is an independent risk in cognitive deficits, but its mechanism remains to be discovered. The protection and mechanism of aerobic interval training （AIT） in hippocampal neuron injury of high fat diet mice are discussed. Methods Forty 2-month-old C57BL/6 mices were randomly divided into control group （Con） ; Con ＋ AIT group; high fat group （HF） and HF ＋ AIT group. Another twenty 2-month-old Sirtuin3 knock out （SIRT3 KO） mice were randomized into HF KO group and HF KO ＋ AIT group. Results Compared with those in control diets, high fat diet for 12 w significantly increased the weight and induced the obesity. The Morris Water-maze training suggested the spatial memory dysfunction in high fat diet group. The level of reactive oxygen species （ROS） and malondialdehyde （MDA） was increased in the HF group, while the activity of Mn superoxide disnautase （MnSOD） and catalase and the expression of SIRT3 were decreased （P 〈 0. 05）. AIT may enhance the SIRT3 expression of hippocampal neuron in HF group, which improved the activity of MnSOD and catalase and alleviated the oxidative stress and injury of cognition ability. However, the protection was suppressed in SIRT3 knock-out mice （P 〈0. 05）. Condusion AIT improves the expression of SIRT3 and the activity of mitochondria anti-oxidative enzyme, which anaeliorates the cognition of high fat diet mice. SIRT3 may be the key factor that AIT suppresses hippocampal neuron injury induced by the high fat diet.