| Summary: | Aim:We aimed to investigate the effect of rosmarinic acid (RA) on cell viability, steatosis, paraoxonase (PON)1, and PON3 protein levels in palmitate-induced non-alcoholic fatty liver disease (NAFLD) model in HepG2 cells.Materials and Methods:To induce an experimental steatosis model, HepG2 cells were incubated with 1 mM palmitate for 24 hours. For the treatment, non-toxic RA concentrations were added to the cell culture medium simultaneously with the palmitate. Cell viability was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay. To evaluate steatosis, intracellular triglyceride levels were measured and the cells were examined microscopically with Oil-Red O staining. PON1 and PON3 protein levels were measured by Western blotting.Results:1 mM palmitate caused a significant decrease in cell viability and a significant increase in triglyceride levels, but it did not significantly change PON1 and PON3 protein levels. RA caused a significant increase in cell viability and a significant decrease in triglyceride levels in the palmitate-treated cells. Similar findings with the triglyceride levels of cells were shown in microscopic examination of cells that were stained with Oil-Red O. RA did not significantly change PON1 and PON3 protein levels in neither non-treated cells nor treated cells with palmitate.Conclusion:Our study showed that RA increases cell viability and decreases steatosis, but it does not change PON1 and PON3 protein levels in palmitate-induced NAFLD model in HepG2 cells.
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