SKF7® Attenuates Lipid Accumulation in HepG2 Cells: Potential Implications for Menopause-Associated Metabolic Dysfunction

Menopause-associated metabolic dysfunction is characterized by increased lipid accumulation, obesity, and an elevated risk of non-alcoholic fatty liver disease, driven by hormonal imbalance and altered lipid metabolism. Hepatic lipid accumulation is a key feature of metabolic dysfunction and can be modelled in vitro using free fatty acid (FFA)-induced HepG2 cells. SKF7®, a standardized aqueous ethanolic extract of Labisia pumila, has emerged as a promising botanical product with lipid-lowering properties. This study aimed to evaluate the effects of SKF7® on hepatic lipid accumulation in HepG2 cells and its potential relevance to menopause-associated metabolic dysfunction. The cytotoxicity of SKF7® (10–1000 µg/ml) was evaluated using the MTT assay. Based on cell viability, concentrations ≤250 µg/ml were selected for subsequent experiments. Hepatic lipid accumulation was induced using sodium oleate (SO) at 0.5 and 1.0 mM conjugated with 1% bovine serum albumin. Preliminary findings identified 1.0 mM SO as the optimal concentration for lipid accumulation. FFA-induced HepG2 cells were subsequently treated with SKF7® for 24 h, and intracellular lipid accumulation was assessed using Oil Red O staining. SKF7® showed no significant cytotoxicity at concentrations ≤250 µg/ml. SKF7® treatment significantly attenuated intracellular lipid accumulation in FFA-induced HepG2 cells, with the most pronounced reduction observed at 250 µg/ml compared with the FFA-induced control group (p < 0.001). Notably, lipid accumulation at 250 µg/ml was not significantly different from the untreated normal group. These findings demonstrate that SKF7® attenuates hepatic lipid accumulation, supporting its potential role in improving hepatic lipid homeostasis and menopause-associated metabolic dysfunction.