Objective        To determ

ine the effect of tumor necrosis factor-α (TNF-α) on lipid accumulation in HepG2 cells and its underlying possible mechanism.       Methods        HepG2 cells were treated with TNF-α (2 or 20 ng/mL)

palmitate (PA

0.08 or 0.2 mmol/L)

and TNF-α plus palmitate (combination of the 2 doses of 2 agents) for 24 h

respectively. The intracellular triglyceride (TG) was measured by enzymatic colorimetric method. Then TNF-α of 20 ng/mL and palmitate of 0.08 mmol/L was chosen for the further experiment. Lipid accumulation in the HepG2 cells was observed with Oil Red O staining. Real-time PCR and Western blot analysis were used to detect the expression of SREBP-1

FAS and ACCα at mRNA and protein levels.       Results        TG level was significantly higher in TNF-α treated cells (0.344±0.093 and 0.329±0.068 μg/μg for the doses of 2 and 20 ng/mL) than in control cells (0.192±0.048 μg/μg

P0.05). And that of the combination treatment cells (TNF-α 2 ng/mL plus PA 0.08 mmol/L: 0.451±0.096

TNF-α 2 ng/mL plus PA 0.2 mmol/L: 0.821±0.257

TNF-α 20 ng/mL plus PA 0.08 mmol/L: 1.032±0.286

TNF-α 20 ng/mL plus PA 0.2 mmol/L: 2.134±1.049 μg/μg) was significant higher than the cells treated by PA alone (PA 0.08 mmol/L: 0.247±0.069

PA 0.2 mmol/L: 0.341±0.031 μg/μg

all

P

0.05). Oil red O staining also showed that TNF-α promoted lipid accumulation in HepG2 cells. The expression of SREBP-1

FAS and ACCα at mRNA and protein levels was significantly higher in TNF-α treatment and the TNF-α plus PA treatment cells than in control cells (

P

0.05).       Conclusion        TNF-α promotes lipid accumulation

and enhances the expression of SREBP-1

FAS and ACCα in HepG2 hepatocytes.