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. 2020 Jan 22;13:185–196. doi: 10.2147/DMSO.S232279

Figure 5.

Figure 5

DHA inhibits NF-κB activation through deacetylation of p65 mediated by Sirt1. (A) A representative set of data from three independent experiments is illustrated (left panel) and quantification histograms (right panel) of Sirt1, Ac-p65, P-p65 and p65 expressions in HepG2 cells. Values are mean±S.E.M. (n = 3, *p < 0.05; **p < 0.01 versus Ctrl cells). (B) Proposed model for DHA regulating hepatic steatosis in liver. DHA inhibits HFD-induced downregulation of Sirt1. On the one hand, accumulation of Sirt1 inhibits NF-kB activation through deacetylating p65. Inactivated NF-kB reduces pro-inflammation, leading to ameliorated hepatic steatosis. On the other hand, increased Sirt1 promotes β-oxidation and TAG export resulting in decreased hepatic steatosis.