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目的探讨过氧化物酶体增殖物激活受体γ(PPARγ)及解偶联蛋白2(UCP2)在非酒精性脂肪性肝病(NAFLD)发病中的作用;观察罗格列酮对实验性NAFLD的治疗效果。方法 60只雄性SD大鼠随机分为对照组,模型组,罗格列酮低剂量及高剂量治疗组。RT-PCR检测肝脏组织PPARγ及UCP2表达情况。结果随着造模时间延长,高脂饮食使大鼠肝脏组织中PPARγm RNA、UCP2m RNA表达逐渐增强(P<0.05);罗格列酮治疗能够下调两者的表达(P<0.05)。结论高脂饮食可使模型大鼠肝脏组织中PPARγ及UCP2表达增强。罗格列酮对非酒精性脂肪性肝病大鼠具有一定的治疗作用,并呈一定的时间-剂量依赖性,其作用可能通过下调肝脏组织中PPARγ及其下游靶基因UCP2的表达来实现。
Objective To investigate the role of peroxisome proliferator-activated receptor γ (PPARγ) and uncoupling protein 2 (UCP2) in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). To investigate the effects of rosiglitazone on the development of NAFLD treatment effect. Methods Sixty male SD rats were randomly divided into control group, model group and rosiglitazone low-dose and high-dose treatment groups. RT-PCR detection of liver tissue PPARγ and UCP2 expression. Results With the prolongation of model making time, the expression of PPARγmRNA and UCP2mRNA in rat liver tissues increased gradually with high-fat diet (P <0.05). Rosiglitazone treatment could down-regulate the expression of both PPARγmRNA and UCP2mRNA in both groups (P <0.05). Conclusion High-fat diet can increase the expression of PPARγ and UCP2 in the liver of model rats. Rosiglitazone has a certain therapeutic effect on non-alcoholic fatty liver disease in rats, and has a certain time-and dose-dependent manner, and its effect may be achieved by down-regulating the expression of PPARγ and its downstream target gene UCP2 in liver tissues.