Objective      To investigate the effect of hepatitis B virus X (HBx) gene silencing on expression of lipid metaboli

sm related genes in HepG2.2.15 cells.       Methods      Cells were divided into a blank control group (HepG2.2.15 cells)

a negative control group (HepG2.2.15 cells transfected with negative HK plasmids)

a shHBx group (HepG2.2.15 cells transfected with shHBx plasmids) and a HepG2 group (HepG2 cells). shHBx plasmid was constructed and transfected into HepG2.2.15 cells using PolyJet

TM

reagent. Expressions of green fluorescent protein and HBx protein were examined under fluorescence microscope and by Western blotting after 24 h-96 h transfection to identify a best interference time. Then cells were treated with sodium oleate for 24 h and 48 h

respectively. Degree of hepatic steatosis was determined by triglyceride (TG) test. mRNA expression of sterol regulatory element binding protein-1c (SREBP-1c) was detected by reverse transcription polymerase chain reaction (RT-PCR)

and protein expressions of liver X receptor alpha (LXRα) and fatty acid synthase (FAS) were detected by Western blotting.       Results      shHBx plasmid was successfully constructed and transfected into HepG2.2.15 cells. Compared with the blank control group and negative control group

HBx protein level decreased significantly in the shHBx group. The lowest level was detected at 48 h-72 hafter transfection (0.337±0.042 vs 0.577±0.032

0.333±0.032 vs 0.654±0.049

P0.01). After cells were stimulated with sodium oleate

the TG content

SREBP-1c mRNA level and LXRα and FAS protein levels increased as the time extended

and they decreased significantly in the shHBx group and HepG2 group as compared with the blank control group and negative control group (TG: 26.51±1.98 μg/mg vs 37.16±6.32 μg/mg; SREBP-1c: 0.418±0.051 vs 0.516±0.037; LXRα: 0.463±0.047 vs 0.630±0.026; FAS: 0.463±0.047 vs 0.630±0.017

P0.01). There was no significant difference between the shHBx group and the HepG2 group (P0.05).       Conclusion       HBx plays an important role in HepG2.2.15 cell steatosis. It may affect the lipid metabolism through regulation of LXRα

FAS and SREBP-1c.