Objective:To explore the effect of oxymatrine on lipid accumulation in HepG2 cells exposed to high fat intervention and to elucidate the molecular mechanism. Methods:Nonalcoholic fatty liver disease(NAFLD)in HepG2 cells was induced by cultured with medium containing 0.25 mmol/L palmitic acid(Pa). The concentrations of triglyceride in HepG2 cells were measured by red oil O staining and triglyceride assay kit. After successful modeling

the Pa-medium group were randomly divided into 3 groups:Pa group(0.25 mmol/L)

metformin(Met)group(0.2 mg/m L)

oxymatrine(Omt)group(0.08 mg/m L). The normal-medium(N)group was established at the same time. After 48 h of drug intervention

the cells were collected respectively. Triglyceride content and the related markers of oxygen stress were measured by kits and 2

7-dichlorofuorescin diacetate(DCFH-DA)staining. The expressions of the key mediators involved in fatty acid transportation and oxidation were examined by real time PCR(q RT-PCR)and Western blot.Results:Red oil O staining and measurement of triglyceride(TG)showed that there were lipid accumulation in HepG2 cells exposedto palmitic acid for 24 h

while the lipid accumulation ameliorated obviously after oxymatrine and metformin administration(POmt=0.023

PMet=0.043). Compared with Pa group

oxymatrine and met formin administration increased the m RNA expression of carnitine palmitoyl transferase-1(CPT-1)(POmt=0.000

PMet=0.000)

and suppressed the m RNA(POmt=0.000

PMet=0.000)and protein(POmt=0.000

PMet=0.000)expression of CD36 simultaneously. After the treatment with oxymatrine and metformin

the generation of reactive oxygen species(ROS)and malondialdehyde(MDA)(POmt=0.016

PMet=0.001)reduced significantly

while the activities of total superoxide dismutase(T-SOD)(POmt=0.007

PMet=0.007)and glutathion peroxidase(GSH-Px)(POmt=0.183

PMet=0.020)increased. Conclusion:Oxymatrine could alleviate lipid accumulation in HepG2 cells exposed to palmitic acid through reducing the long-chain fatty acid uptake

increasing the β-oxydation and improving oxygen stress state.