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首页> 外文期刊>Journal of Nanjing Medical University >Effects of paclitaxel on cell proliferation and apoptosis and its mechanism in human lung adenocarcinoma A549 cells
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Effects of paclitaxel on cell proliferation and apoptosis and its mechanism in human lung adenocarcinoma A549 cells

机译:紫杉醇对人肺腺癌A549细胞增殖和凋亡的影响及其机制

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Objective: To investigate the effect of paclitaxel on cell proliferation and apoptosis of human lung adenocarcinoma A549 cells line and its mechanism in vitro. Methods: Cell growth inhibition of paclitaxel on A549 cells was analyzed by MTT assay. Cell apoptosis was detected by DNA cytofluorometry, Hoechst33258 staining when treated with paclitaxel for 48 hours. Meanwhile, Cell cycle and apoptotic rate were analyzed by flow cytometry. The protein expressions of Bax and Bcl-2 were studied by Western Blot. Results: Paclitaxel inhibited the proliferation of A549 cells in a time-and dose-dependant manner. Hoechst33258 staining indicated that apoptosis was induced by paclitaxel. After treated for 48 hours, cell apoptosis rates of 25 nmol/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 11.52 ± 1.94% ,17.73 ± 2.53% , and 29.32 ± 5.51% respectively, which were significantly higher than those of control group 5.88 ± 1.07% (all P < 0.01), and apoptosis rate increased in dose-dependant manner. Meanwhile, G2/M stage cell percentage of 25 nmol/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 42.52 ± 6.25% , 40.46 ± 5.81%, and 35.34 ± 6.17% respectively, which were significantly higher than that of control group 22.32 ± 3.30% (all P < 0.01); Western blot showed that paclitaxel increased the expression of Bax and decreased the expression of Bcl-2 in dose-dependant manner. Conclusion; Paclitaxel can inhibit A549 cell proliferation in a time- and dose-dependant manner. Its mechanism may be related to arresting cell cycle in G2/M stage and induce cell apoptosis by up-modulating Bax expression arid down-modulating Bcl-2 expression.
机译:目的:探讨紫杉醇对人肺腺癌A549细胞增殖和凋亡的影响及其体外机制。方法:MTT法检测紫杉醇对A549细胞的生长抑制作用。用紫杉醇处理48小时后,通过DNA细胞荧光检测和Hoechst33258染色检测细胞凋亡。同时,通过流式细胞仪分析细胞周期和凋亡率。 Western Blot检测Bax和Bcl-2的蛋白表达。结果:紫杉醇以时间和剂量依赖性方式抑制A549细胞的增殖。 Hoechst33258染色表明紫杉醇可诱导细胞凋亡。处理48小时后,紫杉醇组25 nmol / L,50 nmol / L和100 nmol / L紫杉醇的细胞凋亡率分别为11.52±1.94%,17.73±2.53%和29.32±5.51%,明显高于那些。对照组5.88±1.07%(均P <0.01),且凋亡率呈剂量依赖性增加。同时,紫杉醇组25 nmol / L,50 nmol / L和100 nmol / L的G2 / M期细胞百分比分别为42.52±6.25%,40.46±5.81%和35.34±6.17%,显着高于对照组22.32±3.30%(所有P <0.01); Western blot结果显示紫杉醇以剂量依赖性方式增加Bax的表达而降低Bcl-2的表达。结论;紫杉醇可以以时间和剂量依赖的方式抑制A549细胞的增殖。其机制可能与在G2 / M期阻滞细胞周期有关,并通过上调Bax表达和下调Bcl-2表达诱导细胞凋亡。

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