摘要
目的探讨藤黄酸对人多发性骨髓瘤U266细胞凋亡的影响及机制。方法不同浓度藤黄酸处理U266细胞,四甲基偶氮唑盐(MTT)法检测对细胞增殖的影响,AnnexinⅤ/PI双染法检测细胞的凋亡,JC-1染色法检测线粒体跨膜电位水平,流式细胞仪检测荧光素激活的Caspase3、Caspase8、Caspase9阳性细胞水平。结果藤黄酸呈浓度依赖性抑制U266细胞的生长,藤黄酸>0.5μg/ml才出现较明显的诱导凋亡的能力,藤黄酸降低U266细胞线粒体跨膜电位水平。藤黄酸作用U266细胞24h和48h时激活的Caspase3、Caspase8、Caspase9阳性细胞比例分别上升24.9%、31.7%、32.4%和57.0%、64.5%、63.5%。结论藤黄酸可抑制U266细胞的生长,机制与诱导U266细胞凋亡有关,线粒体跨膜电位途径和胞浆激活途径参与了凋亡的发生。
Objective This study was aimed to investigate the effect of gambogic acid （GA） on the apoptosis of multiple myeloma U266 cell line and its mechanism. Methods The U266 cells were treated with GA at different concentration, the inhibition rates were detected by MrI3＇ assay. Apoptosis induced by GA was observed by Annexin V/PI doubling staining assay. Mitochondrial membrane potential was measured by JC assay. Activated Caspase 3, Caspase 8 and Caspase 9 in living U266 cells were measured by caspGLOWTM fluorescein staining kit. Results U266 cell growth was inhibited in a concentration-dependent manner. GA decreased the mitochondrial membrane potential of U266 cell. GA induced apoptosis of U266 cells and increased activated Caspase 3, Caspase 8, Caspase 9 positive ceil number for 24. 9%, 31.7%, 32.4% in 24 h and 57.0% ,64. 5% ,63.5% in 48 h. Conclusions GA inhibits the growth of U266 cell by the effect of apoptosis, GA triggers U266 cell apoptosis through both intrinsic and extrinsic pathways.
出处
《中华临床医师杂志（电子版）》
CAS
2011年第4期42-45,共4页
Chinese Journal of Clinicians(Electronic Edition)
