ABSTRACT
Objective: To investigate the effect of resveratrol (Res) on the fat synthesis in the liver cancer HepG cells, and to elucidate its possible mechanism. Methods: The HepG cells were cultured in vitro and divided into Res group (treated with 40 umol • L-1 DMSO- diluted Res for 24 h) and control group (treated with the same concentration of DMSO for 24 h). The cell supernatant was collected, and the levels of triglyceride (TG) and total cholesterol (TO in the cells in various groups were measured by ELISA. The mRNA and protein expression levels of lipase synthase acetyl-CoA carboxylase (ACCl), fatty acid synthetase (FASN) and stearoyl-CoA desaturase (SCD1) in the cells in various groups were detected by qRT-PCR and Western blotting method. The levels of O-linked N-acetylglucosamine (O-GIcNAc) glycosylation in the cells in various groups were detected by Western blotting method. Results: Compared with control group, the levels of TG and TC in the cells in Res group were decreased, but the difference was not statistically significant (t1=1.886, P>0.05; t2=2.457,P>0.05). Compared with control group, the levels of expressions of ACCl, FASN and SCD1 mRNA and proteins in the cells in Res group were significantly decreased ( P<0.05 or P<0. 01); the O-GlcNAc glycosylation level in the cells in Res group was significantly decreased (t=2. 87, P<0.05). Conclusion: Res lias the effect of inhibiting the fat synthesis in the liver cancer HepG cells. Its mechanism may be related to the reduction of cellular O-GlcNAc glycosylation level and the reduction of the expression of FASN.
ABSTRACT
Objective: To explore the effects of atorvastatin on the natural antisense transcription of apolipoprotein A1 (apoAl-NAT) in the HepG cells and its influence in the expressions of lipid metabolism related genes. Methods: The HepG cells were intervened with different concentrations (0, 1, 10 and 100 nmol • L-1 ) of atorvastatin, and the 0 nmol • L-1 atorvastatin group was used as control group. The total RNA of HepG cells in various groups were extracted at different time points (6, 12, 24, and 48 h). The mRNA expression levels of lipid metabolism-related genes and apoAl-NAT expression levels were detected by Real-Time PCR method. Results: The morphology of HepG cells in 1 and 10 nmol • L-1 atorvastain groups was normal. Compared with 6 h, the expression levels of apoAl-NAT in the HepG cells in 10 nmol • L atorvastatin group at 12, 24 and 48 h were significantly decreased (P