ILF3 inhibits p-AMPK expression to drive non-alcoholic fatty liver disease progression

Figure 2 Knockdown of ILF3 alleviated lipid deposition in hepatocyte and mice models. A and B: Knockdown of ILF3 reduced triglyceride (TG), aspartate transaminase (AST) and alanine transaminase (ALT) secretion in Oleic acid mixture (OA)-treated HepG2 cells; C: Oil Red O staining showing knockdown of ILF3 Lightens lipid accumulation in OA-treated HepG2 cells; D-F: Knockdown of ILF3 suppressed the proliferation and promoted the apoptosis of hepatocytes; G and H: Knockdown of ILF3 reduced TG, AST and ALT secretion in mice with high-fat diet (HFD) feeding; I: Oil Red O staining shows knockdown of ILF3, which lightens lipid accumulation in liver tissues with HFD feeding. All data are presented as the mean ± SD. ^bP < 0.01; ^cP < 0.001; AST: Aspartate transaminase; ALT: Alanine transaminase; NC: Negative control; shILF3: Small hairpin RNA targeting LF3 intravenously.