白藜芦醇与紫杉醇联合应用对肺癌细胞PC9的杀伤效应

    Killing effect of the application of the resveratrol combined with paclitaxel on lung cancer cell PC9

    • 摘要: 目的:探讨白藜芦醇(RES)联合紫杉醇(PTX)对人肺癌细胞PC9的凋亡作用及其机制。方法:不同浓度的RES和PTX单用和联合作用于PC9细胞后,分别采用四甲基偶氮唑蓝法测定其对PC9的增殖抑制作用,流式细胞术检测其对细胞周期分布和凋亡的影响,Western blot法检测Caspase-3蛋白、抗凋亡蛋白Bcl-2、促凋亡Bax表达的变化。结果:10、20、30 μmol/L的RES和0.001、0.01、0.1 μmol/L的PTX均以时间和浓度依赖方式抑制PC9细胞的增殖,RES联合PTX的抑制率高于RES和PTX单用组(P<0.01)。单用RES和PTX均能诱导PC9细胞发生凋亡和G0/G1期阻滞,两者联合应用,诱导细胞凋亡和G0/G1期阻滞作用显著增强(P<0.01)。Western blot法检测显示在RES和PTX联用之后,Caspase-3蛋白、Bcl-2、Bax的改变显著大于单药作用。结论:RES、PTX均可抑制人肺癌PC9细胞增殖、诱导其凋亡、阻滞细胞G0/G1期、伴随Caspase-3活性上调,且两者联合应用具有协同作用,可显著促进细胞凋亡,其机制可能与上调凋亡蛋白Bcl-2、下调抗凋亡蛋白Bax有关。

       

      Abstract: Objective:To explore the apoptosis-inducing effects of the application of the resveratrol(RES)combined with paclitaxel(PTX)on lung cancer cell line PC9,and its proable mechanism.Methods:After the PC9 cells were co-cultured with the single and combination of different concentrations two drugs,the anti-proliferative effects of drugs were measured using MTT,the cell cycle distribution and apoptosis were detected by flow cytometry,and the protein levels of Caspase-3,Bcl-2 and Bax were detected by western blotting.Results:The effects of RES and PTX on the inhibiting the prolification of PC9 cells were the time- and concentrate-dependent manner.The inhibition rate of RES combined with paclitaxel was higher than that of single RES or PTX use(P<0.01).The single use of RES or PTX could induce the apoptosis and block G0/G1 phase in PC9 cells,and the effect of which was significantly enhanced when two drugs were combined(P<0.01).Western blot assay showed that the changes of Caspase-3,Bcl-2 and Bax after the joint use of RES and PTX were significantly more than that of the single drug use.Conclusions:Both RES and PTX can inhibit the proliferation,induce apoptosis,block G0/G1 phase and increase the Caspase-3 activity of human lung cancer PC9 cells.The combined use of RES and PTX has synergistic effect,which can significantly promote the cell apoptosis,and the mechanism may be related to the upregulation of Bcl-2 and downregulation of Bax.

       

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