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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 peroxisome proliferator - activated receptor γ (PPAR - γ) is involved in the development of nonalcoholic fatty liver disease. Methods Male C57BL / 6J mice were induced to develop non-alcoholic fatty liver disease by standard high-fat diet. Reverse transcription polymerase chain reaction (RT-PCR) and Western Blot were used to detect liver PPAR-γ and fatty acid translocase mRNA The mRNA and protein levels of fatty acid translocase of 1C1C7 hepatoma cells treated with PPAR-γpromoter palmitic acid were detected by RT-PCR and Western Blot, respectively, and compared with the normal diet group. Results The liver tissue PPAR-γ in high-fat diet nonalcoholic fatty liver disease group was significantly higher than that in normal diet control group (1.84 ± 0.16 vs 1.00 ± 0.11, P <0.05), Western Blot showed that protein level was significantly increased; The mRNA level of fatty acid translocase was also significantly higher than that of the normal diet control mice (2.75 ± 0.26 vs 1.00 ± 0.08, P <0.05). Western Blot showed that the protein level was significantly increased. After 200 μM PPAR-γ natural agonist After treated with palmitic acid for 6 h, the mRNA expression level of fatty acid translocase in 1C1C7 cells was significantly higher than that in control group (2.98 ± 0.25 vs 1 ± 0.06, P <0.05). Western Blot showed that the protein level increased significantly. Conclusion PPAR-γ may be involved in the formation of nonalcoholic fatty liver disease by increasing the expression of fatty acid translocase.