Objective        To investigate whether hepatitis B virus X protein (HBx) increases sodium oleate-induced lipid accumulation in HepG2 cells.       Methods       HBX gene eukaryotic expression vector pIRES2-EGFP-HBx was transiently transfected into HepG2 cells to establish HepG2-HBx cell model for HBx expression. HepG2 cells transfected with empty vector pIRES2-EGFP (HepG2-pIRES2) and untransfected HepG2 cells (HepG2) were used as controls. Expression of green fluorescent protein (GFP) was observed by fluorescence microscope after transfection. At 16 h after transfection

each group of cells was treated with sodium oleate for 24 and 48 h (HBx/OA group

empty/OA group and G2/OA group

respectively). Lipid accumulation in each group of cells was observed by triglyceride (TG) content detection and oil red O staining. At 24 h after sodium oleate treatment

RT-PCR and Western blot were applied to measure mRNA levels of sterol regulatory element binding protein-1 (SREBP-1) and liver X receptor alpha (LXRα) and protein levels of HBx

LXRα and fatty acid synthase (FAS)

respectively.       Results       At 16 h after transfection

GFP expression was detected in HepG2-HBx and HepG2-pIRES2 cells

while HBx expression was only detected in HepG2-HBx cells. These suggested that HepG2-HBx cell model for HBx expression was successfully obtained. Compared with those of the control groups

TG and lipid contents were significantly increased in HBx/OA group (P0.01) after the cells treated with sodium oleate. At 24 h after sodium oleate treatment

mRNA levels of LXRα and SREBP-1 as well as protein levels of LXRα and FAS in the HBx/OA group were significantly higher than those in the control groups (P0.01/0.05).       Conclusion        HBx increases the susceptibility of HepG2-HBx cells to factors causing lipid metabolism disorder through up-regulating expressions of lipid synthesis-related genes of HBx-LXRα-SREBP-1/FAS pathway

thereby increasing sodium oleate-induced lipid accumulation in HepG2 cells.