Objective     To observe the role of endoplasmic reticulum stress (ERS) proteins in palmitate sodium-induced apoptosis of human steatotic L02 hepatocytes and study the relation between ERS and apoptosis in steatotic hepatocytes.      Methods     A steatosis model of human L02 hepatocytes was induced by palmitate sodium. Hepatocytes were divided into normal control group and experimental group containing 72 μmol/L palmitate sodium. Optimal palmitate sodium concentration was selected by MTT assay. A triglyceride (TG) kit was used to detect lipid accumulation in hepatocytes with oil red O staining. Apoptosis of hepatocytes was detected by flow cytometry with Annexin V-PE/7-AAD staining. Expression of GRP78

CHOP and P-JNK was tdetected by Western blotting.      Results     Palmitate sodium induced steatosis and apoptosis of L02 hepatocytes in vitro. The apoptosis rate of L02 hepatocytes was significantly higher in experimental group than in control group 48 h after the model was induced by palmitate sodium（5.95±0.37 vs 1.38±0.42

P0.05）. Western blot analysis showed that the expression level of GRP78 was significantly higher at 12 h than at 0 h after the model was induced by palmitate sodium（0.50±0.03 vs 0.37±0.02

P0.05）and reached its peak at 48 h（0.83±0.01）. An almost similar increase was observed in expression of CHOP

P-JNK

and GRP78.      Conclusion     Palmitate sodium is rather lipotoxic to L02 hepatocytes and can induce ERS. ERS up-regulated CHOP and P-JNK expression may play an important role in palmitate sodium-induced apoptosis of steatotic L02 hepatocytes.