Objective: Prevention of inflammation is one of the possible remedy procedure for steatohepatitis during NAFLD. In this study, we researched the folic acid (FA) potency to attenuate the inflammation of palmitate-treated HepG2 cells and the related signalling pathways.
Methods: The molecular mechanisms related to FA anti-inflammatory effect in palmitate and Hcy-treated HepG2 cell line were assessed.
Results: The results indicated that while palmitate enhances the expression and secretion of TNF-α, IL-6, and IL-1β, and also intracellular ROS level, FA at concentrations of 25, 50, and 75 µg/mL significantly reversed these effects in HepG2 cells. In addition, FA could ameliorate inflammation and decrease ROS production induced by Hcy. Furthermore, FA pre-treatment suppress palmitate -induced (NF-κB) p65 level in palmitate or Hcy stimulated cells.
Conclusions: Overall, these results suggest that FA reduces inflammation in HepG2 cells through decreasing ROS and Hcy concentration level resulting in inhibiting the NF-κB pathway.
Keywords: Non-alcoholic fatty liver disease; folic acid; hepatocytes; homocysteine; inflammation; nuclear factor-kappa B; palmitate; reactive oxygen species.