Objective      To detect the expression change of Sec61α in hepatic steatosis and its possible mechanism.       Methods      L02 liver cells were treated with palmitic acid and oleic acid mixture to establish an in vitro cellular model of nonalcoholic fatty liver disease (NAFLD) (steatosis group). Those cells without treatment were assigned into a control group. The steatotic hepatocytes were further incubated with or without a Sec61 inhibitor Eeyarestatin Ⅰ (inhibitor group or DMSO group

respectively). The cells were collected at 0

2

4

8

12

and 16 h after induction for oil red O staining

qRT-PCR

or Western blotting to detect the expression of Sec61α

GRP78

GRP94

and Bcl-2.       Results      Liver cell steatosis was induced by the palmitic acid and oleic acid mixture. As compared to the control group

the hepatocytes in the steatosis group showed a decrease of Sec61α expression in early stages (2 and 4 h

P

0.05)

but an increased in late stages (8 and 12 h

P

0.05). Moreover

GRP78 was up-regulated in 8 h after induction and reached the highest level at 16 h after induction (

P

0.01). Furthermore

Eeyarestatin Ⅰ significantly attenuated hepatocytic steatosis as well as the expression of Sec61α and GRP78 proteins (

P

0.01)

but upregulated GRP94 and Bcl-2 expression (

P

0.01).       Conclusion      Sec61α may be involved in hepatic steatosis by regulating liver cell endoplasmic reticulum stress.