Efect of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells

Non-alcoholic fatty liver disease is a prevalent liver condition that can progress to fibrosis and cirrhosis. It also poses a risk for hepatocellular carcinoma, underscoring the importance of identifying effective treatments. N-acetylcysteine, an inhibitor of glutathione depletion, shows promise in modulating intracellular glutathione biosynthesis and combating oxidative stress, making it a potentially beneficial therapy for liver fibrosis in non-alcoholic fatty liver disease. This study assesses the impact of N-acetylcysteine on HepG2 cells which were induced into fatty liver cells was evaluated. HepG2 cells were cultured in DMEM and seeded onto six-well plates at a density of 5 × 10⁵ cells. Following a 24-h incubation period, the cells were exposed to a medium inducing fat accumulation. Subsequently, the cells were treated with varying concentrations of N-acetylcysteine for 48 h. Some plates were utilized for Real-Time-PCR tests, while others underwent Oil Red staining. The findings indicated a significant increase in the expression of fatty acid β-oxidation genes in the group treated with 10mM N-acetylcysteine (p < 0.05), along with reduced expression of lipogenesis-related genes (p < 0.05) in N-acetylcysteine-treated groups. Analysis of apoptotic gene expression revealed decreased BAX expression but increased BCL2 expression in the N-acetylcysteine-treated groups. Oil Red staining demonstrated a dose-dependent reduction in lipid droplets compared to the control group. This study's results suggest that N-acetylcysteine has the potential to decrease lipid droplets and modulate lipid metabolism effectively.

Graphical abstract