KA2012MBL复合提取液体外抗肿瘤活性评价及相关机制研究

Antitumor activity and mechanism of KA2012MBL in vitro

关键词:  细胞毒  肿瘤多药耐药  细胞周期  线粒体膜电位  细胞凋亡

Key words:  [Key words]　SRB  cytotoxicity  cell life-cycle  mitochondria membrane potential  apoptosis

摘要:

目的　系统评价KA2012MBL复合提取液的抗肿瘤活性及对P-gp介导的肿瘤多药耐药的克服能力，并初步探讨KA2012MBL复合提取液的抗肿瘤机制。方法　应用SRB法测定KA2012MBL复合提取液对K562/A、K562/S和HGC-27的细胞毒活性，应用流式细胞术检测KA2012MBL复合提取液对K562/S细胞的细胞周期阻滞作用、凋亡诱导作用和对其线粒体膜电位的影响作用。结果　KA2012MBL复合提取液对肿瘤细胞株K562/A、K562/S和HGC-27 均具有细胞毒活性，IC50值分别为(1.12±0.15)%(v/v%)、(1.18±0.04)%(v/v%)、(1.21±0.17)%(v/v%),并可有效克服P-gp介导的肿瘤多药耐药。 流式细胞术检测结果显示KA2012MBL复合提取液可有效降低K562/S细胞的线粒体膜电位，并可使K562/S细胞阻滞在G0/G1期，从而诱导其凋亡。 结论　KA2012MBL复合提取液通过诱导肿瘤细胞凋亡而杀死肿瘤细胞，同时能克服P-gp介导的肿瘤多药耐药。要]　目的　系统评价KA2012MBL复合提取液的抗肿瘤活性及对P-gp介导的肿瘤多药耐药的克服能力，并初步探讨KA2012MBL复合提取液的抗肿瘤机制。方法　应用SRB法测定KA2012MBL复合提取液对K562/A、K562/S和HGC-27的细胞毒活性，应用流式细胞术检测KA2012MBL复合提取液对K562/S细胞的细胞周期阻滞作用、凋亡诱导作用和对其线粒体膜电位的影响作用。结果　KA2012MBL复合提取液对肿瘤细胞株K562/A、K562/S和HGC-27 均具有细胞毒活性，IC50值分别为(1.12±0.15)%(v/v%)、(1.18±0.04)%(v/v%)、(1.21±0.17)%(v/v%), 并可有效克服P-gp介导的肿瘤多药耐药。 流式细胞术检测结果显示KA2012MBL复合提取液可有效降低K562/S细胞的线粒体膜电位，并可使K562/S细胞阻滞在G0/G1期，从而诱导其凋亡。 结论　KA2012MBL复合提取液通过诱导肿瘤细胞凋亡而杀死肿瘤细胞，同时能克服P-gp介导的肿瘤多药耐药。

Abstract:

[Abstract] Objective　To evaluate the antitumor activity of KA2012MBL and the ability to overcome P-gp mediated MDR in vitro. Methods　The cytotoxicity of KA2012MBL against K562/A, K562/S and HGC-27 were determined by SRB assay. FACS analysis was used to detect the cell cycle arrest activity and apoptosis induction activity of KA2012MBL on K562/S cells and the loss of mitochondria membrane potential （MMP） of K562/S cells caused by KA2012MBL. Results KA2012MBL showed excellent in vitro cytotoxicity against K562/A,K562/S and HGC-27, with IC50 of (1.12±0.15)%(v/v%),(1.18±0.04)%(v/v%) and (1.21±0.17)%(v/v%),respectively. It also shows ability to overcome P-gp mediated MDR. Furthermore, KA2012MBL caused the loss of MMP of K562/S cells and cell cycle arrest at G0/G1 phase, and induced the apoptosis of K562/S cells. Conclusion　KA2012MBL exerts its antitumor activity by apoptosis induction in tumor cells, which indicates KA2012MBL would show very potent in vivo antitumor activity. Furthermore, KA2012MBL could overcome P-gp mediated MDR successfully.