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目的探讨不同浓度紫杉醇对卵巢癌细胞发挥抗癌效应的内在机制。方法以0.01、0.1、1、10、50μmol/L紫杉醇作用于人卵巢癌细胞系A2780,采用碘化丙啶(PI)单染法流式细胞术检测不同浓度紫杉醇作用下细胞周期的变化情况。进而对细胞进行同步化处理,采用PI单染法流式细胞术分析低浓度(0.01μmol/L)紫杉醇对细胞周期的影响;AnnexinⅤ/PI双染法流式细胞术分析高浓度(50μmol/L)紫杉醇对A2780细胞坏死的影响。结果①紫杉醇浓度为0.1、1、10μmol/L时,G2/M期细胞比例明显高于0.01μmol/L组(P<0.01)和50μmol/L组(P<0.01)。②A2780细胞经同步化处理后给予0.01μmol/L紫杉醇,经过一个细胞倍增时间未观察到G0/G1期阻滞。③0.01μmol/L组,1μmol/L组坏死细胞比例明显低于50μmol/L组(P<0.01)。结论在0.1~10μmol/L的浓度范围内,紫杉醇可能通过诱导G2/M期阻滞使卵巢癌细胞发生凋亡,浓度为0.01μmol/L时紫杉醇诱导凋亡与G0/G1期或G2/M期阻滞均无关,浓度为50μmol/L时紫杉醇可能主要通过诱导细胞坏死发挥抗癌效应。
Objective To investigate the intrinsic mechanism of anticancer effects of paclitaxel on ovarian cancer cells. METHODS: Human ovarian cancer cell line A2780 was treated with 0.01, 0.1, 1, 10, 50 micromol / L paclitaxel. The cell cycle was detected by flow cytometry with propidium iodide (PI) staining. Then the cells were synchronized, the effect of low concentration (0.01μmol / L) paclitaxel on the cell cycle was analyzed by PI single-stained flow cytometry; AnnexinⅤ / PI double staining flow cytometry analysis of high concentration (50μmol / L ) Paclitaxel on A2780 cell necrosis. Results ① The percentage of cells in G2 / M phase was significantly higher than that in 0.01μmol / L group (P <0.01) and 50μmol / L group (P <0.01) at 0.1,1,10μmol / L paclitaxel concentration. ②A2780 cells were treated with 0.01μmol / L paclitaxel after synchronization, and no G0 / G1 arrest was observed after a cell doubling time. ③ The proportion of necrotic cells in 0.01μmol / L group and 1μmol / L group was significantly lower than that in 50μmol / L group (P <0.01). Conclusions Paclitaxel may induce apoptosis of ovarian cancer cells by inducing G2 / M arrest in the concentration range of 0.1 ~ 10μmol / L. When the concentration of 0.01μmol / L paclitaxel induces apoptosis and G0 / G1 phase or G2 / M Stage blockade was not related to the concentration of 50μmol / L paclitaxel may be mainly through the induction of cell necrosis play an anti-cancer effect.