Reduces proinflammatory cytokine levels and increases lipid phagocytosis activity, thereby enhancing lipid scavenging and inhibiting oxidative stress and cellular damage. Alleviates alcohol-induced elevated levels of inflammatory cytokines, regulates p62 and autophagy crosstalk via the Keap-1/Nrf2 pathway, and attenuates hepatic steatosis and inflammatory responses. Improves hepatic bioenergetics, metabolic signaling, and mitochondrial viability. This evidence concerns the gene NFE2L2 and Hepatic steatosis.