期刊文献+

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 被引量:13

GABA Inhibits the Liver Oxidative Stress and Hepatic Steatosis in High-Fat Diet-Fed Obese Mice
下载PDF
导出
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<0.05);添加质量分数0.2%、0.12%和0.06%GABA可显著降低肝脏质量和肝指数,质量分数0.2%、0.12%GABA显著抑制肝脏脂肪变性和改善肝功能(P<0.05)。相比正常组,高脂组动物肝组织中抗氧化酶活性显著降低,自由基和丙二醛含量显著升高(P<0.05);质量分数0.2%、0.12%GABA可显著缓解氧化应激。高脂日粮小鼠肝脏PPARα、Cpt1a和PGC-1α表达显著下调,SREBP-1c、FAS和ACC1表达显著上调(P<0.05),而添加质量分数0.2%、0.12%GABA可显著缓解高脂造成的上述基因表达的变化。因此,高脂日粮导致小鼠肝脏氧化应激、脂肪变性及肝功能损伤,一定剂量GABA可改善肝脏氧化还原状态和脂肪变性,从而预防脂肪肝发生。 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-1αin 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.
出处 《食品与生物技术学报》 CAS CSCD 北大核心 2015年第6期613-620,共8页 Journal of Food Science and Biotechnology
基金 国家"十二五"科技支撑计划项目(2012BAK17B09 2013BAD19B09)
关键词 高脂 氧化应激 脂肪肝 肝脂肪变性 伽马氨基丁酸 high fat oxidative stress fatty liver hepatic steatosis GABA
  • 相关文献

参考文献20

  • 1Powell E E, Cooksley W G, Hanson R, et al. The natural history of nonalcoholic steatohepatitis: a follow-up study of forty-two patients for up to 21 years[J]. I-Iepatology, 1990, 11 ( 1 ) : 74-80. 被引量:1
  • 2Sharabi Y, Eldad A. Nonalcoholic fatty liver disease is associated with hyperlipidemia and obesity[J]. Am J Med, 2000, 109(2) : 171. 被引量:1
  • 3Sekiya M, Yahagi N, Matsuzaka T, et al. Polyunsaturated fatty acids ameliorate hepatic steatosis in obese mice by SREBP- 1 suppression[J]. Hepatology, 2003,38(6) : 1529-1539. 被引量:1
  • 4Shimano H, Horton J D, Shimomura I, et al. Goldstein, Isoform le of sterol regulatory element binding protein is less active than isoform la in livers 0f transgenic mice and in cultured cells [J]. J Ciin Invest, 1997, 99(5) :846 - 854. 被引量:1
  • 5Takahashi N, Senda M, Lin S, et al. Auraptene regulates gene expression involved in lipid metabolism through PPARalpha activation in diabetic obese mice[J]. Mol Nutr Food Res, 2011,55(12) : 1791-7197. 被引量:1
  • 6Zammit V A. Carnitine palmitoyltransferase 1: Central to cell function[J]. IUBMB Life, 2008, 60(5): 347-354. 被引量:1
  • 7St-Pierre J, Drori S, Uldry M, et al. Suppression of reactive oxygen species and neurodegeneration by the PGC- 1 transcriptional zoaetivators[J]. Cell, 2006, 127(2) :397-408. 被引量:1
  • 8XIE Zhenxing, XIA Shufang, LE Guowei. Gamma-aminobutyric acid improves oxidative stress and function of the thyroid in high- fat diet fed mice[J]. J Funet Foods, 2014(8) :76 - 86. 被引量:1
  • 9Low, O H, Rosebrough N J, Fan" A L,et al. Protein measurement with the Folin phenol reagent[J]. J Biol Chem, 1951,193: 265- 275. 被引量:1
  • 10Kobayashi H, Gil-Guzman E, Mahran A M, et al. Quality control of reactive oxygen species measurement by luminol-dependent chemiluminescence assay[J]. J Androl, 2001,22(4) :568-574. 被引量:1

二级参考文献12

  • 1陈新美,王晓华.螺旋藻藻蓝蛋白的稳定性及抗癌活性研究[J].氨基酸和生物资源,2006,28(1):59-62. 被引量:19
  • 2白新鹏,裘爱泳.美味猕猴桃根正丁醇提取物对小鼠急性肝损伤的保护作用[J].食品与生物技术学报,2006,25(6):115-118. 被引量:9
  • 3Hayashi K, Hayashi T, Morita N, et al An extract from Spirulina platensis is a selective inhibitor of herpes simplex virus type 1 penetration into HeLa cells[J]. Phytotherapy Research, 1993,7 ( 1 ) : 76 -- 80. 被引量:1
  • 4Salazar M, Chamorro G, Salazar S, et al. Effect of Spirulina maxima consumption on reproduction and periand postnatal development in rats[J]. Food and Chemical Toxicology, 1996,34 (4) : 353- 359. 被引量:1
  • 5Keppler D, Lesch R, Reutter W, et al. Experimental hepatitis induced by D-galactosamine[J]. Experimental and Molecular Pathology, 1998,9(2) :279--290. 被引量:1
  • 6Reeves P, Nielsen F, Fahey G. AIN-93 purified diets for laboratory rodents: final report of the American Institute of Nutrition ad hoc writing committee on the reformulation of the AIN-76A rodent diet[J]. Journal of Nutrition, 2003,123 (11 ) : 1939--1951. 被引量:1
  • 7Miyake S. The mechanism of release of hepatic enzymes in various liver diseases. II. Altered activity ratios of GOT to GPT in serum and liver of patients with liver diseases[J]. Acta medica Okayama, 1999,33(5): 343--358. 被引量:1
  • 8Anukarahanonta T, Shinozuka H, Farber E. Inhibition of protein synthesis in rat liver by d-galactosamine[J]. Research Communications in Chemical Pathology and Pharmacology, 2003,5 (2) : 481 -- 491. 被引量:1
  • 9Stachlewitz RF, Seabra V, Bradford B, et al. Glycine and uridine prevent d-galactosamine hepatotoxicity in the rat: role of Kupffer cells[J]. Hepatology, 1999,29 (3) : 737 - 745. 被引量:1
  • 10Boindogurong J, Higaki T, Egashira Y, et al. Protective Effect of butylated hydroxyanisole and butylated hydroxytoluene against acetaminophen-induced hepatotoxicity in rats[J]. Journal of Oleo Science,2005,54(3) : 153-159. 被引量:1

共引文献10

同被引文献128

引证文献13

二级引证文献60

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部