nicotinamide-beta-riboside and Liver-Cirrhosis

Increasing nicotinamide adenine dinucleotide (NAD. Mice were injected with CCl. We found NR could prevent liver fibrosis and reverse the existing liver fibrosis. NR inhibited the activation of LX-2 cells induced by TGF-β, activated Sirt1 and deacetylated Smad2/3. Sirt1 knockdown diminished the inhibiting effect of NR on LX-2 cells activation, and increased expressions of acetylated Smads. In conclusion, NR could prevent liver fibrosis via suppressing activation of hepatic stellate cells (HSCs). This protective effect was mediated by regulating the acetylation of Smads signaling pathway.. NR protected mice against liver fibrosis induced by CCl

Topics: Acetylation; Animals; Carbon Tetrachloride; E1A-Associated p300 Protein; Gene Expression Regulation; Hepatic Stellate Cells; Liver Cirrhosis; Male; Mice; Mice, Inbred C57BL; Niacinamide; Protective Agents; Pyridinium Compounds; Sirtuin 1; Smad2 Protein; Smad3 Protein; Transforming Growth Factor beta