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目的研究紫杉醇脂质体联合卡铂对宫颈癌Hela细胞凋亡的影响。方法用设定浓度的紫杉醇(0.5和1μmol/L)单独或联合(0.5和25 mg/L)卡铂分别处理Hela细胞24 h。用MTT比色法检测细胞活力,荧光探针检测细胞内活性氧,用流式细胞仪检测细胞凋亡,用Western blot检测凋亡蛋白p53、Bax和Bcl-2的表达量。结果与空白对照组相比,紫杉醇、卡铂单独处理组可降低细胞活力,提高ROS含量,使p53和Bax蛋白表达升高,降低Bcl-2蛋白表达,使Hela细胞发生凋亡。且紫杉醇联合卡铂对Hela细胞的杀伤作用显著大于单独作用组。结论本实验初步证明紫杉醇和卡铂均通过引起Hela细胞活性氧升高,诱导p53蛋白介导线粒体凋亡通路,导致Hela细胞凋亡的发生,还进一步证明紫杉醇联合卡铂对Hela细胞的杀伤作用显著大于二者单独作用。
Objective To study the effect of paclitaxel liposome combined with carboplatin on the apoptosis of cervical cancer Hela cells. Methods Hela cells were treated with paclitaxel (0.5 and 1 μmol / L) at a concentration of either alone or in combination (0.5 and 25 mg / L) for 24 h. Cell viability was detected by MTT assay. Fluorescence probe was used to detect intracellular reactive oxygen species (ROS). Flow cytometry was used to detect apoptosis. Western blot was used to detect the expression of p53, Bax and Bcl-2. Results Compared with the blank control group, paclitaxel and carboplatin alone could reduce the cell viability, increase the content of ROS, increase the expression of p53 and Bax, decrease the expression of Bcl-2 and induce the apoptosis of Hela cells. The killing effect of paclitaxel combined with carboplatin on Hela cells was significantly greater than that of the single treatment group. Conclusions This experiment proves that both paclitaxel and carboplatin can induce the apoptosis of Hela cells by inducing the increase of reactive oxygen species (ROS) in Hela cells and inducing the p53 protein-mediated mitochondrial apoptosis pathway, further demonstrating the killing effect of paclitaxel and carboplatin on Hela cells Significantly greater than the two alone.