Role and mechanism of miRNA-181a in nonalcoholic fatty liver disease

Abstract

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.