Objectiveâ‘ To observe Synergistic effect of the compound herbal medicinal prescription of Supplementing qiã€Nourishing yi and resolving du serological pharmacology and 5-FU on apoptosis of HepG2 cell in vitro.â‘¡To observe the effect of herbal medicinal prescription on protein expression of survivin and activity of caspase3 induced by 5-FU. Thereby, to investigate mechanism of Synergistic effect of the compound herbal medicinal prescription and 5-FU.Methods Blood were collected from SD rats that were treated with the Chinese herbal medicine. Then medicated serum prepared from this blood were used to culture with HepG2 cells, It is divided to Medicated serum group; 5-FU group; Medicated serum +5-FU group and Blank serum was taken as control, HepG2 cells were administrated to different group. After 24hã€48hã€72h, Growth activity was measured by MTT. Apoptosis was detected by Flow Cytometry, respectively. Activity of caspase3 was investigated by Quantitative Assay. Survivin protein expression was detected by Western-blot.Resultâ‘ The apoptosis and proliferation of HepG2 cells were not observed in Medicated serum group and Control group.â‘¡More apoptosis of HepG2 cells were observed in 5-FU+ Medicated serum group than in 5-FU group after 48h and 72h(P<0.05).â‘¢After 24hã€48hã€72h, there were no marked change of survivin protein expression and caspase3 activity in Medicated serum group and control group, It showed that expression of survivin and activity of caspase3 increased gradually in 5-FU group and in 5-FU+ Medicated serum group, But there were significant differene between 5-FU group and 5-FU+Medicated serum group(P<0.05), The level of survivin expression in 5-FU+ Medicated serum group were less than in 5-FU group (P<0.05), the activity of caspase3 in 5-FU+Medicated serum group were more than in 5-FU group(P<0.05).Conclusion This Chinese medicine contained serum of Supplementing qi and Nourishing yin and resolving du could increase the level of apoptosis through decreasing expression of inhibitor apoptosis protein of survivin, and to weaken the inhibition of caspase3 activity caused by survivin, then to enhance the sensitivity of HepG_2 cells to chemotherapy. |