紫杉醇对人肺腺癌细胞系A549生长抑制作用的研究

目的:评价紫杉醇对肺腺癌细胞A549的生长抑制作用,以及诱导凋亡与G2-M期阻滞的关系。方法:紫杉醇不同浓度、不同时间分别处理A549细胞,采用MTT试验和流式细胞术进行检测及分析。结果:紫杉醇对A549的细胞毒性呈时间依赖性(P<0.05),10~1 000 nmol/L的浓度对A549生长的影响差异不显著(P>0.05)。紫杉醇浓度≤100 nmol/L时,G2-M期细胞的比率随浓度增加而增高(P<0.05);凋亡的比例在低浓度范围内(0.1~10 nmol/L)呈浓度依赖性,浓度进一步增加,反而降低。10 nmol/L作用时,凋亡的发生呈时间效应;1 000 nmol/L作用时,G2-M期阻滞表现出时间效应,但不如低浓度诱导凋亡出现的早。紫杉醇诱导的凋亡和G2-M期阻滞无相关性(P>0.05)。结论:紫杉醇对A549的生长抑制作用呈时间依赖性,但在一定浓度范围内剂量效应不明显;低浓度紫杉醇虽然对G2-M期阻滞的影响较小,但却能比高浓度更早诱发凋亡,延长作用时间亦可达到有效抑制肿瘤细胞增殖的目的。

study of paclitaxel on growth-inhibiting effects for human lung adenocarcinoma A549 cells

Objective:To assess the growth-inhibiting effects of paclitaxel on human lung adenocarcinoma A549 cell line in vitro.Methods:A549 cells were exposed to paclitaxel at different concentration or different treating time,then the growth inhibiting effects of the cell line were detected with MTT assay,and the change of the cell cycle and apoptosis were analyzed with flow cytometry.Results:The growth inhibition effect of paclitaxel on A549 cells was time dependent(P<0.05).The inhibition effects caused by paclitaxel from 10 nmol/L to 1 000 nmol/L had no significant difference(P>0.05).At the concentration-dependent experiment,the proportion of apoptosis was highest at 10 nmol/L paclitaxel,while the percentage of G_(2)-M phase increased in accordance with raise of the paclitaxel concentration,when paclitaxel concentration changed from 0.1 nmol/L to(100 nmol/L)(P<0.05).At the time-dependent experiment,the inducement of apoptosis was time dependent(P<0.05) and the percentage of G_2-M phase was highest at 12 h when paclitaxel was 10 nmol/L.At 1 000 nmol/L paclitaxel,G_2-M arrest was time dependent(P<0.05),but its function to apoptosis was later than 10 nmol/L's.Apoptosis had no relationship with G_2-M arrest((P>0.05)).Conclusion:Paclitaxel inhibits the growth of A549 cells in vitro in time-dependent manner.It can induce apoptosis and G_2-M arrest but the late two have no relationship between each other.Low concentration paclitaxel can also inhibit effectively the growth of A549 cells by prolonging treatment.