Effect Of Fatty Acid-CoA Ligase 4 Inhibitor Triacsin C On The Proliferation And Apoptosis In HepG2 Cells In Vitro

Objective: To investigate the effect of fatty acid-CoA ligase 4(FACL4) inhibitor Triacsin C on the proliferation and apoptosis in HepG2 cells in vitro.Methods: Human hepatoma cells line HepG2 was cultured in vitro. Streptavidin-peroxidase(S-P) immunocytochemical method was used to detect the expression of FACL4 protein in HepG2 cells. The effects of Triacsin C on the growth and survival of HepG2 cells were determined by MTT assay and growth curve assay. Apoptosis was determined using hematoxylin- eosine(HE)staining and flow cytometry.Results: S-P immunocytochemical results revealed that FACL4 protein was located in the cytoplasm of HepG2 cells. Triacsin C could inhibite the growth of HepG2 significantly. The cells were treated with varies concentrations of Triacsin C(500,1000,1500,2000)μg/L for up to 24 hr, 48hr and 72hr. The inhibitory rates of the cells were 24.48±3.63%,29.61±2.28%,35.43±3.36%,39.16±2.53% in 24 hours; 32.83±2.17%,49.88±2.49%,53.53±2.64%,57.91±3.06% in 48 hours and 49.99±3.23%, 54.21±3.15%,61.39±2.21%, 68.07±4.14% in 72 hours, respectively. There was significant difference between treated groups and control cells in different times(p<0.01) and various concentrations(p<0.01). At the same time, flow cytometry revealed that Triacsin C could induce the apoptosis of HepG2 cells in a concentration-dependent manner and the apoptosis rate was 19.47±0.12%, 20.40±0.10%, 20.90±0.17%, 24.67±0.21% with various concentrations of Triacsin C (500, 1000, 1500, 2000)μg/L in 48 hours. It was significantly higher than that of control cells (1.93±0.23%, p<0.01).Conclusion:1, FACL4 is overexpression in HepG2 cells. 2, Triacsin C can inhibite proliferation in a concentration and time-dependent manner in HepG2 cells.3, Triacsin C can induce apoptosis in a concentration-dependent manner in HepG2 cells.