Objective       To determine the role of autophagy in the inhibitory effect of resveratrol (RSV) on hepatic steatosis.       Methods       Human hepatoma cell line HepG2 were treated by 0.2 mmol/L sodium palmitate (palmitic acid sodium

PA) for 24 h to establish a cell model of hepatic steatosis

followed by the treatement of 40 μmol/L RSV with or without 5 mmol/L 3-methyladenine (3-MA)

a specific inhibitor of autophagy

for another 24 h. In this way

the cells were divided into 4 groups

a control group

PA group

PA+RSV group and PA+3-MA+RSV group. After incubation terminated

CCK-8 assay was used to detect the cell viability

oil red O staining was employed to detect the intracellular lipid accumulation

and the cell lipid content was measured by a lipid quantitative colorimetric test kit. In order to monitor autophagy in HepG2 cells

laser confocal microscopy was used to observe the lysosomes

transmission electron microscopy (TEM) was used to detect the autophagosomes

and Western blotting was used to detect the expression of autophagy marker protein MAP1LC3B2.       Results      PA of 0.2 mmol/L and RSV of 40 μmol/L had no significant effect on the proliferation of HepG2 cells (P0.05). However

PA treatment significantly increased lipid accumulation in the HepG2 cells

and RSV treatment significantly enhanced the expression level of hepatocyte MAP1LC3B2

the number of lysosomes and autophagosomes. Simultaneouly

RSV treatment notably reduced the lipid accumulation of HepG2 cells induced by PA. Furthermore

3-MA treatment obviously inhibited the above effect of RSV.       Conclusion       RSV improves hepatocyte fatty degeneration caused by PA through inducing autophagy.