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目的:探讨miRNA-181a(miR-181a)对非酒精性脂肪性肝病的影响及其可能的机制。方法:使用棕榈酸处理HepG2细胞构建非酒精性脂肪性肝病细胞模型,检测细胞内miR-181a的表达及脂质沉积。用转化生长因子-β处理细胞检测其对miR-181a表达的影响。通过调控HepG2细胞miR-181a的表达水平,分别检测转染miR-181a模拟物和抑制物后HepG2细胞内miR-181a表达、脂质沉积和还原型谷胱甘肽和活性氧水平。通过实时荧光定量PCR和蛋白质印迹法对生物信息学预测的miR-181a靶基因进行验证。两组独立样本间比较采用独立样本n t检验,多组间比较资料特征符合正态分布且方差齐性,采用单因素方差分析。n 结果:棕榈酸处理后HepG2中脂质沉积明显增多,miR-181a表达水平显著高于对照组。HepG2细胞转染miR-181a抑制物后,miR-181a表达下调,甘油三酯和活性氧下降,还原型谷胱甘肽升高,预测靶基因沉默信息调节因子2相关酶1的mRNA和蛋白表达量上调;而转染miR-181a模拟物后,结果与上述改变相反。结论:miR-181a参与非酒精性脂肪性肝病的脂质沉积并促进脂质过氧化,miR-181a可能是通过抑制沉默信息调节因子2相关酶1的表达来影响非酒精性脂肪性肝病的发病机制及进展。“,”Objective:To investigate the role and probable mechanism of miRNA-181a in nonalcoholic fatty liver disease.Methods:HepG2 cells were treated with palmitic acid to construct a nonalcoholic fatty liver disease cell model, and the expression of miR-181a and lipidosis in the cells were measured. Transforming growth factor-β (TGF-β) was used to examine the effect of miR-181a expression in HepG2 cells. The miR-181a, lipidosis, reduced glutathione and reactive oxygen species (ROS) were determined by controlling and regulating the miR-183 expression levels after transfection with miR-181 mimics and inhibitors in HepG2 cells. The miR-181a target genes were predicted by bioinformatics analysis, and verified by real-time fluorescent quantitative PCR and western blotting. The independent sample t-test was used for the comparison between the two independent samples, and the comparison between multiple groups were accorded with the normal distribution, homogeneity of variance, and one-way analysis of variance.Results:Lipidosis was significantly increased after palmitic acid treatment in HepG2 cells, and the expression level of miR-181a was significantly increased than control group. After HepG2 cells were transfected with miR-181a inhibitors, the expression of miR-181a, triglycerides and reactive oxygen species were down-regulated, and reduced glutathione, predicting the mRNA and protein expression of target gene silencing information regulator 2 related enzyme 1 were up-regulated. However, the results were contrary to the above changes after transfection with miR-181a mimics.Conclusion:miR-181a participates in lipidosis and promotes lipid peroxidation in nonalcoholic fatty liver disease. miR-181a may affect the pathogenesis and progression of nonalcoholic fatty liver disease by inhibiting the expression of silencing information regulator 2 related enzyme 1.