In the current study, we demonstrated that AO promoted autophagy flux and alleviated liver steatosis in an HFSW-fed NAFLD mouse model and OAPA-treated mouse primary hepatocytes by inducing the phosphorylation of AMPK and TFEB, which subsequently increased the expression of targets involved in lipid degradation and decreased the expression of targets involved in lipid biosynthesis. The gene discussed is TFEB; the disease is metabolic dysfunction-associated steatotic liver disease.