Thirdly, in a similar model system, SB was found to ameliorate O-linked β-N-acetylglucosamine O-GlcNAcylation associated with the NF-κB signalling pathway and led to decreased inflammation [92] and to enhanced AO defence associated with the upregulation of Nrf2, suppression of NF-κB signalling and decreased expression of proinflammatory cytokines to ameliorate hepatic steatosis and fibrosis [93]. This evidence concerns the gene NFKB1 and Hepatic steatosis.