RESUMEN
Objective: To investigate the effects of oxaliplatin combined with capecitabine on the expressions of tumor-related factors in the gastric cancer tissue and the levels of serum inflammatory factors in the rats with experimental gastric cancer, and to elucidate the possible mechanism of their anti-tumor effects. Methods: Sixty Wistar rats were randomly divided into control group∗ model group∗ oxaliplatin group∗ capecitabine group and oxaliplatin combined with capecitabine group (combination group); there were 12 rats in each group. The BGC823 cells were used to establish the experimental gastric cancer models. The experimental rats were given capecitabine (400 mg • kg ) and (or) oxaliplatin (20 mg • kg ) at the same time; the rats in control group and model group were given the normal saline at the same volume for 8 weeks. The average tumor weight was measured after administration. The apoptosis of gastric cancer cells was measured by TUNEL staining. The protein expression levels of P53. signal transduction and activation factor 3 (STAT3) and vascular endothelial growth factor (VEGF) in the gastric cancer tissue of the rats in various groups were detected by Western blotting method. The levels of serum interleukin-6 (IL-6)» interleukin-10 (IL-10) and tumor necrosis factor-a (TNF-a) of the rats in various groups were detected by ELISA. Results: Compared with control group, the protein expression levels of P53» STAT3. and VEGF in the gastric cancer tissue and the levels of serum IL-6. 11,-10. and TNF-a of the rats in model group were significantly increased (P<0. 05). Compared with model group, the average tumor weights and the protein expression levels of P53» STAT3. and VEGF in the gastric cancer tissue and the levels of serum IL-6. IL-10. and TNF-a of the rats in oxaliplatin group, capecitabine group and combination group were significantly decreased (P∗C0. 05); the apoptosis indexes (AI) of gastric cancer cells were significantly increased (P<0. 05). The average tumor weight, the protein expression levels of P53∗ STAT3∗ and VEGF in gastric cancer tissue and the levels of serum IL-6. IL-10. and TNF-a of the rats in combination group were significantly lower than those in capecitabine group and oxaliplatin group ( P-C0. 05). Conclusion: Both oxaliplatin and capecitabine can paly the antitumor effects by reducing the protein expression levels of the tumor-related factors and the serum IL-6. IL-10. and TNF-a levels of the gastric cancer rats, and the anti-tumor effect of combined utilization is better than that of capecitabine or oxaliplatin used alone.
RESUMEN
Objective: To investigate the effects of silymarin on the proliferation, migration and invasion of human gastric cancer cell line SGC 7901 and its role in promoting apoptosis, and to clarify their possible mechanisms. Methods: The human gastric cancer SGC 7901 cells in logarithmic growth phase were selected and divided into control group (without silymarin) and different concentrations (15, 30, and 60 mg · L-1) of silymarin groups. Inverted microscope was used to observe the morphology of cells. MTT method was used to detect the cell cycle and the apoptotic rates of cells in various groups. The inhibitory rates of proliferation of cells in various groups were detected by flow cytametry. Scratch test and Trans well chamber assay were used to detect the cell migration and invasion abilities. Results: After the SGC 7901 cells were treated with silymarin for 24 h, compared with control group, the adherent densities of the cells in 30 and 60 mg · L-1 silymarin groups were smaller, the cell shape was irregular and the volume was smaller, resulting in a large number of cell debris. Compared with control group, the inhibitory rates of cells in different concentrations of silymarin groups were increased significantly (P<0. 05); the percentages of cells in Gi phase and the apoptosis rates of SGC 7901 cells were increased significantly (P<0. 05); the migration distances were decreased (P<0. 05) and the number of transmembrane cells was decreased significantly (P<0. 05). Conclusion: Silymarin can inhibit the proliferation of human gastric cancer SGC 7901 cells by inducing the G1 phase cell arrest and early apoptosis.