食品与生物技术学报
食品與生物技術學報
식품여생물기술학보
JOURNAL OF FOOD SCIENCE AND BIOTECHNOLOGY
2015年
6期
613-620
,共8页
谢振兴%李秀%耿旭%夏淑芳%乐国伟%施用晖
謝振興%李秀%耿旭%夏淑芳%樂國偉%施用暉
사진흥%리수%경욱%하숙방%악국위%시용휘
高脂%氧化应激%脂肪肝%肝脂肪变性%伽马氨基丁酸
高脂%氧化應激%脂肪肝%肝脂肪變性%伽馬氨基丁痠
고지%양화응격%지방간%간지방변성%가마안기정산
high fat%oxidative stress%fatty liver%hepatic steatosis%GABA
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。
研究伽馬氨基丁痠(GABA)對高脂日糧小鼠肝髒氧化應激、脂肪變性及脂代謝相關基因錶達的影響。採用50隻C57BL/6雄性小鼠,隨機分為5組:正常組(正常日糧),高脂組(高脂日糧),3箇GABA處理組(飲水中分彆添加質量分數0.2%、0.12%和0.06%GABA)。實驗18週後,測定小鼠肝髒組織自由基水平、抗氧化酶活性、脂肪和糖原含量以及血漿穀丙轉氨酶、穀草轉氨酶活性,同時對肝組織形態進行觀察,併用RT-PCR檢測肝髒SREBP-1c、FAS、ACC1、PPARα、Cpt1a和PGC-1α的錶達。結果顯示,高脂日糧顯著升高小鼠肝髒質量、肝指數、肝髒甘油三酯和膽固醇含量,降低肝髒功能(P<0.05);添加質量分數0.2%、0.12%和0.06%GABA可顯著降低肝髒質量和肝指數,質量分數0.2%、0.12%GABA顯著抑製肝髒脂肪變性和改善肝功能(P<0.05)。相比正常組,高脂組動物肝組織中抗氧化酶活性顯著降低,自由基和丙二醛含量顯著升高(P<0.05);質量分數0.2%、0.12%GABA可顯著緩解氧化應激。高脂日糧小鼠肝髒PPARα、Cpt1a和PGC-1α錶達顯著下調,SREBP-1c、FAS和ACC1錶達顯著上調(P<0.05),而添加質量分數0.2%、0.12%GABA可顯著緩解高脂造成的上述基因錶達的變化。因此,高脂日糧導緻小鼠肝髒氧化應激、脂肪變性及肝功能損傷,一定劑量GABA可改善肝髒氧化還原狀態和脂肪變性,從而預防脂肪肝髮生。
연구가마안기정산(GABA)대고지일량소서간장양화응격、지방변성급지대사상관기인표체적영향。채용50지C57BL/6웅성소서,수궤분위5조:정상조(정상일량),고지조(고지일량),3개GABA처리조(음수중분별첨가질량분수0.2%、0.12%화0.06%GABA)。실험18주후,측정소서간장조직자유기수평、항양화매활성、지방화당원함량이급혈장곡병전안매、곡초전안매활성,동시대간조직형태진행관찰,병용RT-PCR검측간장SREBP-1c、FAS、ACC1、PPARα、Cpt1a화PGC-1α적표체。결과현시,고지일량현저승고소서간장질량、간지수、간장감유삼지화담고순함량,강저간장공능(P<0.05);첨가질량분수0.2%、0.12%화0.06%GABA가현저강저간장질량화간지수,질량분수0.2%、0.12%GABA현저억제간장지방변성화개선간공능(P<0.05)。상비정상조,고지조동물간조직중항양화매활성현저강저,자유기화병이철함량현저승고(P<0.05);질량분수0.2%、0.12%GABA가현저완해양화응격。고지일량소서간장PPARα、Cpt1a화PGC-1α표체현저하조,SREBP-1c、FAS화ACC1표체현저상조(P<0.05),이첨가질량분수0.2%、0.12%GABA가현저완해고지조성적상술기인표체적변화。인차,고지일량도치소서간장양화응격、지방변성급간공능손상,일정제량GABA가개선간장양화환원상태화지방변성,종이예방지방간발생。
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.