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目的探讨双氢青蒿素(DHA)是否能增加肺腺癌A549细胞对三氧化二砷(ATO)的敏感性及可能的机制。方法以人肺腺癌A549细胞为研究对象,按处理方式分为对照组、单独DHA或ATO处理组及二者联合组,采用MTT比色法检测DHA和ATO对细胞增殖的影响,彗星实验检测DNA损伤情况,荧光探针检测细胞内活性氧(ROS)水平,流式细胞术检测细胞周期和细胞凋亡。结果与ATO单独处理相比,DHA和ATO联合处理可以显著降低A549细胞存活率,同时显著增加细胞尾部DNA百分率和Olive尾距(OTM)、ROS水平和凋亡率(P<0.05);另外,2种处理方式均可以阻滞细胞于G2/M期,但差异无统计学意义(P>0.05)。结论 DHA可以增强ATO杀死肺腺癌A549细胞的敏感性,其机制可能是DHA和ATO联合处理诱导了细胞内ROS的产生与蓄积,ROS可以引起DNA链断裂,进而阻滞细胞周期进行修复,修复失败的细胞最终走向凋亡。
Objective To investigate whether dihydroartemisinin (DHA) can increase the sensitivity of lung adenocarcinoma A549 cells to arsenic trioxide (ATO) and its possible mechanism. Methods Human lung adenocarcinoma A549 cells were divided into control group, DHA or ATO alone group and combination group. The effects of DHA and ATO on cell proliferation were detected by MTT colorimetric assay. Comet assay DNA damage was detected by fluorescence probe. The level of reactive oxygen species (ROS) was detected by fluorescent probe. The cell cycle and apoptosis were detected by flow cytometry. Results Compared with ATO alone, the combination of DHA and ATO significantly decreased the survival rate of A549 cells and significantly increased the ratio of tail DNA, OTM, ROS and apoptosis (P <0.05). In addition, Both treatments could block cells in G2 / M phase, but the difference was not statistically significant (P> 0.05). Conclusion DHA can enhance the sensitivity of ATO to kill lung adenocarcinoma A549 cells. The mechanism may be that the combined treatment of DHA and ATO induces intracellular ROS production and accumulation. ROS can cause DNA strand breaks and then block cell cycle repair, Repairing failed cells eventually goes to apoptosis.