伽马氨基丁酸抑制高脂诱导肥胖小鼠肝脏氧化应激及肝脂肪变性
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伽马氨基丁酸抑制高脂诱导肥胖小鼠肝脏氧化应激及肝脂肪变性

GABA Inhibits the Liver Oxidative Stress and Hepatic Steatosis in High-Fat Diet-Fed Obese Mice

DOI:10.3969/j.issn.1673-1689.2015.06.008

中文关键词: 高脂 氧化应激 脂肪肝 肝脂肪变性 伽马氨基丁酸

英文关键词: high fat, oxidative stress, fatty liver, hepatic steatosis, GABA

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作者

单位

谢振兴

食品科学与技术国家重点实验室江南大学江苏 无 锡 214122

河南大学 医学院河南 开封 475001

李秀

江南大学 食品学院江苏 无锡 214122

耿旭

河南大学 医学院河南 开封 475001

夏淑芳

江南大学 食品学院江苏 无锡 214122

乐国伟

食品科学与技术国家重点实验室江南大学江苏 无 锡 214122

江南大学 食品学院江苏 无锡 214122

施用晖

食品科学与技术国家重点实验室江南大学江苏 无 锡 214122

江南大学 食品学院江苏 无锡 214122

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中文摘要:

研究伽马氨基丁酸(GABA)对高脂日粮小鼠肝脏氧化应激、脂肪变性及脂代谢相关基因表达的影响。采用 50只C57BL/6 雄性小鼠,随机分为5组:正常组(正常日粮),高脂组(高脂日粮),3个GABA处理组(饮水中分别添加质量分数0.2%、0.12%和0.06% GABA)。 实验18周后,测定小鼠肝脏组织自由基水平、抗氧化酶活性、脂肪和糖原含量以及血浆谷丙转氨酶、谷草转氨酶活性,同时对肝组织形态进行观察,并用 RT-PCR检测肝脏SREBP-1c、FAS、ACC1、PPARα、Cpt1a 和 PGC-1α的表达。结果显示,高脂日粮显著升高小鼠肝脏质量、肝指数、肝脏甘油三酯和胆固醇含量,降低肝脏功能(P

英文摘要:

The effects of gamma-aminobutyric acid (γ-aminobutyric acid, GABA) on oxidative stress, liver function, hepatic steatosis and lipid metabolism-related gene expression were studied in the liver of high-fat diet fed mice. 50 C57BL / 6 male mice were randomly divided into five groups: normal group (normal diet), high fat diet group (high fat diet), and three GABA groups (0.2%, 0.12% and 0.06 % GABA in drinking water, respectively). After 18 weeks, reactive oxygen species (ROS) levels, antioxidant enzyme activities, contents of lipid and glycogen in liver and plasma activities of alanine aminotransferase and aspartate aminotransferase were measured. In addition, the morphological features of liver tissue were observed and the expressions of SREBP-1c, FAS, ACC1, PPARα, Cpt1a and the PGC-1α in liver were measured by using of RT-PCR. The results showed that in high-fat diet fed mice, liver weight, liver index, triglyceride and cholesterol contents in liver increased significantly with damaged liver function; 0.2%, 0.12% and 0.06% GABA treatments can significantly reduce liver weight and liver index; 0.2%, 0.12% GABA treatments significantly inhibited hepatic steatosis and improved liver function. Compared with that of in normal group, high fat diet treatment significantly reduced antioxidant enzyme activities and increased ROS and malondialdehyde (MDA) contents; 0.2% and 0.12% GABA treatments significantly alleviated oxidative stress. In liver of high-fat diet fed mice, expressions of PPARα, Cpt1a PGC-1α were significantly reduced, while, expressions of SREBP-1c, FAS and ACC1 were remarkably increased, but both 0.2% and 0.12% GABA supplements can significantly alleviate the gene expression changes that high fat caused. Thus, high-fat diet treatment led to oxidative stress in liver, steatosis and damaged liver function. Meanwhile, a certain dose of GABA can improve redox status and fat metabolisms, thereby preventing the occurrence of fatty liver.

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