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

Figure 3 Knockdown of ILF3 alleviated non-alcoholic fatty liver disease progress by activating the AMPK pathway in vitro. A and B: Knockdown of ILF3 was helpful to phosphorylation of the AMPK pathway in Oleic acid mixture (OA)-treated HepG2 cells detected by Western blotting; C: Oil Red O staining showing knockdown of ILF3 decreased lipid deposition in OA-treated HepG2 cells, while CompoudC reversed this effect; D and E: Knockdown of ILF3 reduces triglyceride, alanine transaminase and aspartate transaminase secretion in OA-treated HepG2 cells, while CompoudC reversed this effect. All data are presented as the mean ± SD. ^aP < 0.05; ^cP < 0.001; AST: Aspartate transaminase; ALT: Alanine transaminase; NC: Negative control; shILF3: Small hairpin RNA targeting LF3 intravenously.