Objective        To investigate the relationship of the expression of protein kinase Cδ (PKCδ) with fatty degeneration and endoplasmic reticulum stress in the steatotic hepatocytes

and investigate the role of PKCδ in pathogenesis of non-alcoholic steatohepatitis (NASH).       Methods        The steatosis model of human L02 hepatocytes was established by induction with fatty a

cid mixture. Triglyceride (TG) kit was used to measured lipid accumulation in the hepatocytes with Oil Red O staining. The expression of PKCδ

binding immunoglobulin protein (Bip)

and spliced X-box binding protein 1 (XBP-1) at mRNA and protein levels were analyzed by real-time PCR and Western blotting respectively. After transient transfection of PKCδ siRNA was used to knock down PKCδ expression in L02 cells

the above expression was detected again.       Results        Fatty acid mixture (oleate-to-palmitate at 2∶1) induced hepatic steatosis

the average LD area per cell of fatty acid 16 h group was 333.06±42.36 pixels

which was apparently more than that of the control group (14.47±9.28)

and TG content was significantly higher than in control group (30.86±6.24 vs 2.30±0.62 μg/mg

P

0.05). Fatty acid mixture up-regulated the expression of PKCδ

Bip and XBP-1 in a time-dependent manner (

P

0.05). Knock-down of PKCδ gene expression led to a reduction in both lipid accumulation [(30.92±1.29)% vs (55.32±6.58)%

P

0.05

]

and the expression of Bip and XBP-1 during fatty acid mixture-induced hepatic steatosis.       Conclusion        PKCδ may play an important role in the prognosis of NASH. Silencing the gene expression of PKCδ can reduce the degree of fatty degeneration and endoplasmic reticulum stress.