Sargentodoxa cuneata combined with chemotherapy drug 5-fluorouracil inhibits growth of liver cancer cells / 中草药

ABSTRACT

Objective To investigate the effect of Sargentodoxa cuneata extracts combined with 5-fluorouracil on the growth inhibition of human hepatoma HepG2 cells, and explore its mechanism. Methods HepG2 cells were cultured in vitro and treated with different concentrations of S. cuneata extracts. The effect of S. cuneata extracts on cell growth inhibition was detected by MTT assay, and the subsequent experimental concentration was selected. HepG2 cells were randomly divided into four groups control group, S. cuneata extracts group (40 mg/L), 5-fluorouracil (10 μmol/L) group, and combination group (S. cuneata extracts 40 mg/L + 5-fluorouracil 10 μmol/L). Cell proliferation inhibition rate was detected by MTT assay and cell cycle was detected by flow cytometry. The expression levels of nuclear antigen PCNA, Cyclin D1, and cell cycle-dependent protein kinase CDK4 were detected by Western blotting. Results The results of MTT assay showed that S. cuneata extracts inhibited the proliferation of HepG2 cells in a concentration-dependent manner (P < 0.05), and S. cuneata extracts with a concentration of 40 mg/L was selected for subsequent experiments. Compared with the control group, the cell proliferation inhibition rate of the S. cuneata extracts group and the 5-fluorouracil group was significantly increased, the proportion of G0/G1 phase cells was significantly increased, and the proportion of cells in the S phase and G2/M phase was significantly decreased (P < 0.05). The protein expression levels of PCNA, Cyclin D1, and CDK4 in the cells were significantly decreased (P < 0.05). Compared with the 5-fluorouracil group, the combination group significantly inhibited the proliferation of HepG2 cells, blocked the cell cycle, and inhibited the protein expression of PCNA, Cyclin D1, and CDK4 in the cells (P < 0.05). Conclusion S. cuneata extracts combined with 5-fluorouracil enhances the growth inhibition of hepatocellular carcinoma HepG2 cells, and its mechanism may be related to the inhibition of the protein expression of PCNA, Cyclin D1, and CDK4 related to the expression levels of PCNA, Cyclin D1, and CDK4 in the inhibited cells.