中文摘要：

目的 比较研究番荔枝内酯大花紫玉盘素（uvarigrin）诱导多药抗药性KBv200细胞及其亲本KB细胞凋亡及其机制。方法 以MTT法进行细胞毒测定；用AnnexinVFITC染色及流式细胞仪检测细胞凋亡。活性氧（ROS）测定以DCFH-DA标记，细胞线粒体跨膜电位（△ψm）测定用DiOC6标记，均以流式细胞仪检测。Caspase-9激活的测定用Western blotting法。结果 大花紫玉盘素对KBv200细胞及其亲本KB细胞的生长均有明显的抑制作用；大花紫玉盘素不仅能介导KB细胞凋亡，而且也能介导KBv200细胞凋亡；大花紫玉盘素作用于KBv200细胞及其亲本KB细胞12，24和48h，均引起ROS升高以及△ψm降低，而且呈时间依赖性。Western blotting方法分析显示Caspase-9被激活。结论 大花紫玉盘素可能通过线粒体通路诱导细胞凋亡。

英文摘要：

Aim To study the effect of uvarigrin on mitoehondrial dependent pathway apoptosis induced by it in MDR KBv200 cells and their parental sensitive KB cells. Methods during the MTT assay was used to detect the cytotoxic effect of uvarigrin on KBv200 and KB cells. Annexin V FITC staining identified uvarigrin-induced apoptosis in KBv200 and KB ceils. These ceils underwent incubation with DCFH-DA, or DiOC6, followed by flowcytometry for the measurement of reactive oxygen species （ROS） and mitochondrial membrane potential （△ψm）, respectively. The Western blotting analysis was performed on Caspase-9 activation. Results Uvarigrin inhibited the growth of KBv200 ceils and KB ceils in vitro. Most of the uvarigrin-induced cells death was found to be due to apoptosis, as determined by Annexin V FITC staining. During the apoptosis, the level of ROS increased while the level of △ψm decreased in a time-dependent manner. Uvarigrin triggered Caspase-9 activation. Conclusion Uvarigrin induced apoptosis in KBv200 cells and KB cells probably through a mitochondria-dependent pathway.