Abstract: Objective The aim of this experiment was to explore the effect and underlying mechanism of curcumin on oleic acid-induced steatosis of HepG2 cells in vitro. Methods HepG2 cells were treated with or without 1 mmol/L oleic acid (OA) to establish nonalcoholic fatty liver disease (NAFLD) cell model. The HepG2 cells were divided into four groups, e.g. control (con), steatosis model (OA) , curcumin control and curcumin-intervened groups. Bodipy493/503 staining was used to detect the distribution of lipid droplets in the HepG2 cells. The ultrastructure of mitochondria was examined by transmission electron microscopy. Reactive oxygen species (ROS) levels were detected by DCFH-DA. The TNF-α and IL-6 levels in the supernatants were measured by a commercial kit. The apoptosis was determined by Hoechst 33258 staining. Western blott was applied to determine the expression of Bcl-2, Bax, mCytc, NF-κB, and Caspase-3/9 proteins. Results Compared with in the control cells, the cells treated with OA showed significantly increased lipid droplets accumulation, while the cells treated with curcumin showed reduced lipid droplets accumulation; the mitochondrial damage including mitochondrial swelling and vesiculation in OA group was more obvious than that in control group, while the mitochondrial damage treated by curcumin was significantly improved; the TNF-α and IL-6 levels in OA group were much higher than that in the control group , while they decreased greatly in curcumin-inervened group ; the ROS levels was (52.24±5.11)% in OA group, significantly higher than (6.71±2.31)% in the control group, while it decreased to (37.44±7.21)% in curcumin-treated group (P<0.05); the apoptosis rate in OA group was (12.12±0.72)%, significantly higher than (2.04±0.57)% in the control group, while it decreased significantly in curcumin-treated group ; the expressions of Bax, NF-κB and cleaved-Caspase-3/9 intensified, and Bcl-2 and mCytc decreased greatly in OA group as compare to those in the control, while the expressions of Bax, NF-κB and Caspase-3/9 decreased, and Cytc and Bcl-2 increased (P<0.05) in curcumin-intervened group. Conclusion Curcumin effectively prevent oleic acid-induced steatosis in HepG2 cells, which might be related to the alleviation of inflammatory reaction, oxidative stress and inhibition of apoptosis.

Key words: HepG2 cells, Nonalcoholic fatty liver disease, Curcumin, Apoptosis, Oxidative stress