Fig. 5. Schematic representation of the potential mechanism of action of RBN against the features of metabolic failures in the liver. RBN inhibited excess TG accumulation in hepatocytes owing its p300 inhibitory activity. RBN potentially binds to the HAT binding domain of p300 and attenuates its catalytic activity. Furthermore, RBN abrogates recruitment of p300 to the CD38 promoter region and consequently inhibits hyperacetylation of H3K9, which is necessary for the gene expression. Finally, the RBN-mediated downregulation of CD38 induces inhibition of TG accumulation and improves insulin sensitivity in the liver. Thus, RBN represents a promising candidate dietary compound for the prevention of metabolic failure in the liver. The chemical structure of RBN was generated using ACD/ChemSketch (Freeware; Ver. 2021. 1. 3).
© Biomolecules & Therapeutics
