Abstract
Pinocembrin-7-O-β-d-glucoside (PCBG), pinocembrin (PCB), and 5-methoxy-pinocembrin-7-O-β-d-glucoside (MPG) are three flavonones isolated from Penthorum chinense Pursh (P. chinense). The effects of the three flavonones on hepatic steatosis and their molecular mechanisms in HepG2 cells were investigated in this study for the first time. A model of hepatic steatosis in HepG2 cells was induced by free fatty acid (FFA), and co-treated with the three flavonones as mentioned. Intracellular lipid droplets were detected by Oil Red O staining. PCB, PCBG, and MPG suppressed oxidative stress by decreasing malondialdehyde (MDA) levels and increasing superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. The levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were ameliorated. Moreover, these flavonones enhanced the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of silent mating type information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator-activated receptor α (PPARα), and reduced the expression of sterol regulatory element binding protein-1c (SREBP1c) and the downstream targets fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and stearoyl-CoA desaturase 1 (SCD1). Molecular docking was used to predict the interaction and combination patterns between the three flavonones and the enzymes above. The results revealed that the SIRT1/AMPK pathway is involved in the functions of the three flavonones, and the most effective flavonone against hepatic steatosis might be PCBG, followed by MPG and PCB. Therefore, the three flavonones from P. chinense were found to exert preventive effects against hepatic steatosis by regulating the SIRT1/AMPK pathway.
Highlights
(PCB), and 5-methoxy-pinocembrin-7-O-β-D-glucoside (MPG) are three flavonones isolated from Penthorum chinense Pursh (P. chinense)
The results revealed that the SIRT1/AMPK pathway is involved in the functions of the three flavonones, and the most effective flavonone against hepatic steatosis might be PCBG, followed by MPG and PCB
To investigate the resistant effects of PCBG, PCB, and MPG on Non-alcoholic fatty liver disease (NAFLD) and their possible therapeutic mechanism, targets on the SIRT1/AMPK/sterol regulatory element binding protein-1c (SREBP1c) pathway related to lipid metabolism were evaluated in a nonalcoholic injured HepG2 cell model induced by free fatty acid (FFA) in the present study
Summary
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world [1]. AMPK stimulation during fatty acid metabolism is presented as AMPK phosphorylation, and it is known as a critical regulator for sterol regulatory element binding protein-1 (SREBP1) activation and lipogenesis [14,15]. Sterol regulatory element binding protein-1c (SREBP1c) regulates gene expression related to glucose metabolism, fatty acid, and lipid production, and its activity is regulated by insulin [16]. Pinocembrin-7-O-β-D-glucoside (PCBG), pinocembrin (PCB), and 5-methoxy-pinocembrin-7-O-β-D-glucoside (MPG) are three flavonones with similar nuclear structures isolated from the extract of P. chinense. To investigate the resistant effects of PCBG, PCB, and MPG on NAFLD and their possible therapeutic mechanism, targets on the SIRT1/AMPK/SREBP1c pathway related to lipid metabolism were evaluated in a nonalcoholic injured HepG2 cell model induced by FFA in the present study. We hypothesized that the flavonones in P. chinense produced their hepatoprotective action via the regulation of lipid generation and metabolism, and in vivo research will be performed in our group
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