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...

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Veröffentlicht in:Journal of molecular histology 2025-02, Vol.56 (1), p.27
Hauptverfasser: Gholamrezapour, Mohammadreza, Taghizadeh Ghavamabadi, Raziyeh, Taghavi, Mohammad Mohsen, Dehghani Soltani, Samereh, Shabanizadeh, Ahmad, Vazirinejad, Reza, Taghipour, Zahra
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Sprache:eng
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Zusammenfassung: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 × 10 5 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 
ISSN:1567-2379
1567-2387
1567-2387
DOI:10.1007/s10735-024-10313-2