高脂肪饮食诱发的C57BL/6J小鼠非酒精性脂肪性肝病肝脏PPAR-γ表达升高

Increased hepatic PPAR-γlevel in C57BL /6J mice with high fat diet induced nonalcoholic fatty liver disease

目的探讨过氧化物酶体增殖物激活受体γ(PPAR-γ)是否与非酒精性脂肪性肝病的形成有关。方法通过标准高脂肪饮食诱导雄性C57BL/6J小鼠形成非酒精性脂肪性肝病,用逆转录聚合酶链式反应(RT-PCR)及Western Blot检测肝脏的PPAR-γ和脂肪酸转位酶mRNA和蛋白水平;用RT-PCR及Western Blot检测PPAR-γ的天然激动剂棕榈酸处理后的小鼠1C1C7肝癌细胞的脂肪酸转位酶mRNA和蛋白水平,并与正常饮食组进行比较。结果高脂肪饮食非酒精性脂肪性肝病组小鼠肝脏组织PPAR-γ显著高于正常饮食对照组小鼠(1.84±0.16 vs 1.00±0.11,P<0.05),Western Blot显示蛋白水平显著升高;脂肪酸转位酶的mRNA水平也显著高于正常饮食对照组小鼠(2.75±0.26 vs 1.00±0.08,P<0.05),Western Blot显示蛋白水平显著升高;经过200μM的PPAR-γ的天然激动剂棕榈酸处理6 h后,1C1C7细胞的脂肪酸转位酶mRNA表达水平显著高于对照组(2.98±0.25vs 1±0.06,P<0.05),Western Blot显示蛋白水平显著升高。结论 PPAR-γ可能通过提高脂肪酸转位酶表达参与非酒精性脂肪性肝病的形成。

Objective To investigate whether PPAR-γplays a role in the pathogenesis of nonalcoholic fatty liver disease in mice. Methods Nonalcoholic fatty liver disease was induced in C57 BL /6J mice via standardized high fat diet. The mRNA and protein levels of PPAR-γand fatty acid translocase were determined by reverse transcription polymerase chain reaction（ RT-PCR） and Western Blot,respectively.Results The mRNA levels of hepatic PPAR-γand fatty acid translocase in the mice with nonalcoholic fatty liver disease were significantly higher than those with normal diet（ 1. 84 ± 0. 16 vs 1. 00 ± 0. 11,P 〈0. 05;2. 75 ± 0. 26 vs 1. 00 ± 0. 08,P 0. 05）. So were the protein levels. The hepatoma cell line 1c1c7 treated by palmitic acid（ 200 μmol /L,for 6h） had a higher mRNA level of fatty acid translocase as compared with normal control（ 2. 98 ± 0. 25 vs 1. 00 ± 0. 06,P〈 0. 05）. So was the fatty acid translocase protein level.Conclusions PPAR-γmay play a role in the pathogenesis of nonalcoholic fatty liver disease in mice through the up-regulation of fatty acid translocase.