Objective    To clarify the expression change and significance of Sigma-1 receptor (Sigma-1R) in non-alcoholic fatty liver disease (NAFLD).     Methods

    An

in-vitro

NAFLD model was established by inducing the steatosis of HepG2 cells using palmitic acid. The cells were collected at the time points of 0

2

4

8 and 12 h

and the steatosis levels were measured by Nile red staining. The expressions of Sigma-1R and endoplasmic reticulum stress marker-glucose regulating protein 78 (GRP78) were detected by real-time PCR and Western blotting. The cell viability change during the steatosis process was detected using 3-(4

5-dimethylthiazol-2-yl)-2

5-diphenyltetrazolium bromide (MTT) assay.     Results    The steatosis of HepG2 cells was induced by fatty acid

and the steatosis levels were increased with the increase of time points. The average steatosis area in the 12-h group (435.14±39.87) was significantly higher than that in the 0-h group (

P

<

0.01). The relative expression levels of GRP78 mRNA in the 8-h and 12-h groups (2.35±0.51 and 8.71±1.20) were significantly higher than that in the 0-h group (

P

<

0.05). However

the relative expression level of Sigma-1R mRNA was significantly decreased in the 2-h group (0.19±0.02 and

P

<

0.05). The protein expression levels of GRP78 in the 8-h and 12-h groups (25.59±0.51 and 28.43±1.20) were significantly up-regulated as compared to that in the 0-h group

while the protein expression levels of Sigma-1R in the 8-h and 12-h groups (15.92±0.42 and 10.73±0.63) were significantly down-regulated as compared to that in the 0-h group (

P

<

0.05). The MTT detection showed that the cell viability during the steatosis process was gradually decreased. The cell viability in the 12-h group [(59.86±4.47)%

]

was significantly decreased as compared to that in the 0-h group (

P

<

0.05).     Conclusion    The low expression of Sigma-1R may induce the endoplasmic reticulum stress during the NAFLD process

and further result in the injury of liver cells.