miR-192-5p regulates lipid synthesis in non-alcoholic fatty liver disease through SCD-1

Figure 1 Hepatic miR-192-5p and SCD-1 levels in rat models. H&E staining of livers (A), body weight (B), hepatic TG levels (C), hepatic miR-192-5p levels (D), and SCD-1 protein levels (E) in rats fed an HFD and treated with liraglutide. The data are expressed as the mean ± SEM (n = 10 rats/group), ^bP < 0.01.

Figure 2 PA induces a decrease in miR-192-5p and an increase in SCD-1 in Huh7 cells. A: The cytotoxic effects of PA on Huh7 cells by the CCK-8 test; B: Cellular TG levels; C: Oil red O staining; D: MiR-192-5p levels; and E: SCD-1 protein levels in Huh7 cells treated with PA. The data are expressed as the mean ± SEM, ^aP < 0.01.

Figure 3 SCD-1 is a direct target of miR-192-5p. A: The binding sites of miR-192-5p with the 3’ UTR of SCD-1; B: The dual luciferase activity in the wild type and mutant SCD-1 3’ UTRs in 293T cells treated with miR-192-5p mimic and inhibitor, respectively. The mRNA (C) and protein levels (D) of SCD-1 in Huh7 cells transfected with miR-192-5p mimic and inhibitor. The data are expressed as the mean ± SEM, ^bP < 0.01.

Figure 4 MiR-192-5p alleviates lipid accumulation in PA-treated Huh7 cells. Oil red O staining (A), cellular TG levels (B), and SCD-1 protein levels (C) in Huh7 cells transfected with miR-192-5p mimic and its negative control followed by exposure to PA. The data are expressed as the mean ± SEM, ^bP < 0.01.

Figure 5 SCD-1 knockdown alleviates the promoting effect of the miR-192-5p inhibitor on lipid accumulation. The protein level of SCD-1 (A), Oil red O staining (B), and cellular TG levels (C) in Huh7 cells transfected with miR-192-5p inhibitor and SCD-1 siRNA followed by exposure to PA. The data are expressed as the mean ± SEM, ^bP < 0.01.