Role and mechanism of miRNA-181a in nonalcoholic fatty liver disease
10.3760/cma.j.cn501113-20200527-00279
- VernacularTitle:miRNA-181a在非酒精性脂肪性肝病中的作用及其机制
- Author:
Ruixian HUANG
1
;
Xiaoyan DUAN
;
Xiaolin LIU
;
Haixia CAO
;
Yuqin WANG
;
Jiangao FAN
;
Baocan WANG
Author Information
1. 上海交通大学医学院附属新华医院消化科，上海 200092
- Keywords:
Non-alcoholic fatty liver disease;
miR-181a;
Transforming growth factor;
Sirtuin1
- From:
Chinese Journal of Hepatology
2021;29(12):1177-1181
- CountryChina
- Language:Chinese
-
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.
