MicroRNA-185 regulates expression of lipid metabolism genes and improves insulin sensitivity in mice with non-alcoholic fatty liver disease

Figure 2 Effect of miR-185 on lipid metabolism in HepG2 cells. HepG2 cells were transfected with pre-miR-185 or anti-miR-185 (an antisense oligonucleotide against miR-185), and fatty acid oxidation and sterol synthesis rates were determined. A: The sterol synthesis rate was determined by the amount of [¹⁴C] acetate incorporated into HepG2 cell sterols after transfection with pre-miR-185; B: The fatty acid oxidation rate was measured by the oxidation of [1-¹⁴C] oleate into ¹⁴CO₂ after transfection with pre-miR-185; C: Sterol synthesis rates in HepG2 cells after transfection with miR-185 inhibitors; D: Fatty acid oxidation rates in HepG2 cells after transfection with miR-185 inhibitors; E: Quantitative reverse transcription-PCR was used to assess the mRNA levels of key lipid metabolism-associated genes in HepG2 cells after overexpression of miR-185; F: mRNA levels of lipid metabolism-associated genes after miR-185 inhibition. Data are mean ± SEM from three separate experiments. ^aP < 0.05, ^bP < 0.01 vs the normal control group. miR-185: microRNA-185; ASO: Antisense oligonucleotide; SREBP-1C: Sterol-regulatory element-binding proteins 1C; SREBP-2: Sterol-regulatory element-binding proteins 2; HMGCR: 3-hydroxy-3-methylglutaryl-CoA reductase.