中文摘要：

目的观察高果糖饮食诱导的小鼠脂肪肝和肝脏氧化应激的发生时程变化,并探讨高果糖饮食致小鼠脂肪肝与氧化应激的关系。方法 60只雄性C57BL/J6小鼠随机分为对照组、高果糖组,分别在喂养3 d、8周后测定小鼠空腹血糖（FBG）、空腹血清胰岛素（FINS）及肝脏甘油三酯（TG）含量,并测定各组小鼠肝脏氧化应激相关指标即丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）及过氧化氢酶（CAT）水平的变化。结果喂养3 d后,与对照组相比,高果糖组小鼠的FBG、FINS无明显变化（P〉0.05）,而肝脏TG显著增加（P〈0.01）;喂养8周后,与对照组相比,高果糖组FBG、FINS、TG均显著增加（P〈0.01）;喂养3 d后,与对照组相比,高果糖组的MDA、SOD、GSH-Px以及CAT水平均无明显变化（P〉0.05）;喂养8周后,高果糖组的肝内MDA明显增加（P〈0.01）,SOD、GSH-Px及CAT活性均显著降低（P〈0.01）。结论短期和长期高果糖喂养均可引起肝内脂质沉积,但短期高果糖喂养引起的肝脏脂质沉积不伴有氧化应激;长期高果糖喂养引起的肝脏脂质沉积伴有氧化应激,提示氧化应激与高果糖饮食诱导的脂肪肝发生发展有关,但介导机制有待进一步研究。

英文摘要：

Objective To observe the time course changes of fatty liver and hepatic oxidative stress induced by high-fructose feeding in mice and to investigate the relationship between fatty liver and liver oxidative stress. Methods A total of 60 male C57 BL / J6 mice were randomly divided into control group（ n = 30） and high-fructose feeding group（ n = 30）. After feeding for 3 d and 8 weeks,the contents of fasting blood glucose（ FBG）,fasting serum insulin（ FINS）and liver triglyceride（ TG） were respectively detected,and related index changes of oxidative stress such as malondialdehyde（ MDA）,superoxide dismutase（ SOD）,glutathion peroxidase（ GSH-Px） and catalase（ CAT） were also detected.Results Compared with those in control group,in high-fructose feeding group,after feeding for 3 d,there were no changes in FBG and FINS levels（ P〉0. 05）,while hepatic TG content was significantly increased（ P〈0. 01）; after feeding for 8 weeks,the FBG,FINS and TG levels were significantly increased（ P〈0. 01）; after feeding for 3 d,there were no changes in MDA,SOD,GSH-Px and CAT levels（ P〈0. 05）; after feeding for 8 weeks,the hepatic MDA level was significantly increased（ P〈0. 01）,while the SOD,GSH-Px and CAT levels were significantly decreased（ P〈0. 01）.Conclusion Both short-term and long-term high-fructose feeding can induce hepatic lipid deposition. However,oxidative stress can not be found in short-term high-fructose feeding,but it can be found in long-term one,which indicates that oxidative stress is associated with fatty liver induced by high-fructose feeding,while its mechanisms should be further studied.