Abstract: Objective: To evaluate the effects of camellia oil on lipid metabolism in free fatty acid-induced HepG2 hepatocytes. Methods: To screen the optimal concentration of action, the effect of camellia oil on HepG2 activity was assessed by CCK-8 assay. HepG2 cells were exposed to different concentrations of camellia oil for 24 h, after which the cells were treated with 0.5 mmol/L free fatty acids for 24 h to induce in vitro model of liver steatosis. Then, intracellular lipid content was detected using Oil Red O staining. Lipid profiles were measured by commercial kits. The mRNA expression of genes related to lipid metabolism was measured by qRT-PCR to investigate the effects and possible mechanisms of camellia oil in regulating lipid metabolism. Results: Compared with the normal control group, fatty acids induction significantly increased the contents of triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) (P<0.05), and decreased the content of high-density lipoprotein cholesterol (HDL-C) (P<0.05). Interestingly, camellia oil pretreatment significantly reversed the changes in intracellular contents of TG, HDL-C and LDL-C induced by fatty acids incubation (P<0.05). In addition, compared with the model group, camellia oil pretreatment significantly decreased the mRNA expression of fatty acid transporter (CD36), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), sterol regulatory element-binding protein-1c (SREBP-1c), and peroxisome proliferator-activated receptor γ (PPARγ) (P<0.05), and increased the mRNA expression of adipose triglyceride lipase (ATGL), peroxisome proliferator-activated receptor alpha (PPARɑ), and carnitine palmitoyltransferase-1A (CPT1A) (P<0.05). Conclusions: Camellia oil may alleviate the lipid metabolism disorder induced by free fatty acids in HepG2 cells partly by modulating the expression levels of genes involved in lipid lipogenesis and oxidation.