Investigating the Effects of Curcumin on Lipid Metabolism and Cell Viability in HepG2 Cells: Potential Therapeutic Implications for Nonalcoholic Fatty Liver Disease

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD), poses a significant global health challenge, necessitating novel therapeutic strategies. This study investigates examines the efficacy of curcumin (Cur), a natural bioactive compound, in suppressing inhibiting the proliferation of hepatocellular carcinoma proliferation and reducing lipid accumulation in vitro. HepG2 cells were treated with Cur (1.25–10 μg/mL) for 24–72 h, revealing a dose- and time-dependent reduction in viability, with an IC50 of 10 µg/mL at 72 h. Oil Red O staining demonstrated Cur's lipid-lowering effects, reducing lipid content by 57% at 5 µg/mL and 78% at 10 µg/mL, suggesting enhanced efficacy at higher concentrations. Quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR) analysis revealed that Cur downregulated key lipogenic regulators Peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBP-α) by 2.3- and 1.8-fold, respectively, while modulating 14-3-3γ/β expression, implicating these pathways in its mechanism. These findings highlight Cur's potential to attenuate hepatic lipid accumulation and cancer cell growth in vitro, warranting further validation in primary hepatocytes and preclinical models to advance its therapeutic prospects for Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).