摘要
目的：探讨紫杉醇体外抑制人黑色素瘤细胞（A375细胞）增殖及诱导凋亡作用机制。方法：四甲基偶氮唑蓝（MTT）还原法测定细胞活力；光镜和电镜观察细胞形态变化；流式细胞术（FCM）检测细胞周期和凋亡率。结果：紫杉醇通过诱导细胞凋亡抑制A375细胞生长。并呈时间和剂量依赖性（P〈0．01）；当0．01-1μmol／L紫杉醇作用于培养细胞24h后即可引起猾亡小体等典型细胞凋亡形态学改变；FCM分析显示：紫杉醇在0．001μmol／L即可诱导细胞凋亡，但不影响细胞周期，在0．01μmol／L时使G0／G1期细胞明显减少，在0．1μmol／L以上时使细胞发生G2／M期阻滞。结论：紫杉醇具有抑制A375细胞生长和诱导细胞凋亡作用。不同浓度紫杉醇诱导细胞凋亡的作用机制不同。
Objective： To investigate the growth- inhibitory and apoptosis-inducing effect of paclitaxel on human melanoma A375 cell and its mechanism in vitro. Methods： The proliferation of A375 cells was determined by using MTT method. The morphological changes of the cells were observed under light and electron microscopes. Cell cycle progression and apeptosis ratio were determined by using flow cytometry. Results： Paditaxel inhibited the growth of A375 cells by inducing apeptosis in a both time-dependent and dosedependent manner （ P 〈 0. 01 ）. The typical morphological changes such as apoptotic body formation were found at 24 hours after A375 cells were exposed to paclitaxel of 0.01 to 1μmol/L. Paclitaxel of 0.001μmol/L was the lowest dose to induce A375 cell apeptosis but did not change cell cycle progression. Paclitaxel of 0. 01μmol/L mainly acted on A375 cells of G0/G1 phases. Paclitaxel of 0. 1 to 1μmol/L induced the cell cycle arrest in G2/M phases. Conclusion. Paclitaxel could inhibit the proliferation and induce the apeptosis of A375 cell in vitro. Paclitaxel of different concentrations may induce the apeptosis by different mechanisms.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2006年第2期134-136,F0002,共4页
Journal of China Medical University
基金
辽宁省科技计划基金资助项目(2003225007-3)
关键词
紫杉醇
黑色素瘤
凋亡
paclitaxel
melanoma
apoptosis
