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

Figure 4 Knockdown of ILF3 alleviated non-alcoholic fatty liver disease progress by activating the AMPK pathway in vivo. A and B: Western blotting showing knockdown of ILF3 helped activate the AMPK pathway in liver tissues; C: Oil Red O staining showed knockdown of ILF3 decreased lipid deposition in liver tissues, while CompoudC reversed this effect; D and E: Knockdown of ILF3 reduced triglyceride, alanine transaminase and aspartate transaminase secretion in mice with high-fat diet feeding, while CompoudC reversed this effect; F: Knockdown of ILF3 was helpful to upregulate pAMPK expression, while CompoudC can reverse this effect. 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.