Effect Of Astragalus Polysaccharide Combined With Cispiatin On Hunman Lung Cancer A549 Cells Proliferation Inhibition And Bax, Bcl-2 And Caspase-3 Effects

Objectives In order to observe the inhibitory effects of two drugs combined astragalus polysaccharides and cisplatin on the lung adenocarcinoma A549 cells’ proliferation, cycle regulation, apoptosis induction and synergistic mechanism of the two drugs, which provided new methods and established theoretical basis for the future clinical application on non-small cell lung cancer chemotherapy.Methods Lung adenocarcinoma A549 cells were cultured in vitro,then selected the cells in logarithmic growth phase experiments were divided into four groups: the negative control group,the astragalus polysaccharide group,the cisplatin group, the Astragalus polysaccharide and cisplatin groups.MTT assay was performed to detect the effects of astragalus polysaccharides, cisplatin and the two combination on cell proliferation, then the joint effects of two medicines evaluated by the Q-value formula. The impact of each group of cell cycle and apoptosis rate are analyzed by flow cytometry. The mRNA expression of apoptosis-related protein Bcl-2, Bax and Caspase-3 levels was detected by RT-PCR.Western blot was used to detect the protein expression of Bax, Bcl-2 and Caspase-3.Results 1.Astragalus polysaccharides, or cisplatin and or the doublet could inhibit lung adenocarcinoma A549 cells’ proliferation on concentration and time-dependent manner. The combination on inhibition was superior to single medicine, but the synergistic and additive antitumor effect of the combination on the A549 cells.2. After treated the A549 cells with different groups for 48 h, the results showed that astragalus polysaccharides and cisplatin could respectively arrest cell cycles in G1 and S phase(P<0.01), while the combination could arrest cell cycles in G1, S phases(P<0.01). Astragalus polysaccharides and cisplatin could induce apoptosis of the A549 cells and the apoptosis rate of the combination was superior to single medicine(P<0.01). 3. Astragalus polysaccharides and cisplatin can promote expression of Bax and Caspase-3 mRNA, while the expression of Bcl-2 mRNA were statistically significant(P<0.01). Compared to single drug group, astragalus polysaccharides and Cisplatin effect was stronger, the differences were statistically significant(P<0.01). 4. Compared to the negative control group, astragalus polysaccharides and cisplatin could significantly promote human lung cancer A549 cells Bax, Caspase-3 protein expression, whereas inhibition expression of Bcl-2 protein. Compared to the negative control group and single drug group, astragalus the combined effects of polysaccharides with cisplatin effect was stronger, the differences were statistically significant(P<0.01).Conclusions Astragalus polysaccharides and cisplatin inhibit the proliferation of human lung adenocarcinoma A549 cells and promote apoptosis, the effect of which combination significantly enhanced. Astragalus polysaccharides and cisplatin synergistically enhance the pro-apoptotic effects on lung adenocarcinoma A549 cells, and its mechanism may be associated with reduced expression of Bcl-2, up-regulated expression of Bax and Caspase-3.