姜黄油诱导人肝癌细胞凋亡及其机制  

Turmeric oil induces human hepatoma cell apoptosis via mitochondrial pathway

作　　者：雷慧[1] 谭佳妮[2] 李绍平[3] 李海涛[1] 季晖[2] 

机构地区：[1]南京中医药大学药理学教研室,南京210046 [2]中国药科大学药理学教研室,南京210009 [3]澳门大学中华医药研究院

出　　处：《中国药科大学学报》2013年第3期263-266,共4页Journal of China Pharmaceutical University

摘　　要：探讨姜黄油的抗肝癌作用及其作用机制,采用二甲基噻唑蓝比色法(MTT)检测肝癌细胞的活力,流式细胞仪检测细胞凋亡率以及线粒体膜电位的变化,Western blot方法检测凋亡相关蛋白Bax、Bcl-2、caspase-3、caspase-9以及细胞色素C的表达。结果发现,姜黄油能时间依赖性地抑制肝癌细胞的生长,降低线粒体膜电位并诱导其凋亡;升高细胞内Bax与Bcl-2的比值;诱导细胞色素C从线粒体中的释放并激活caspase-9和caspase-3。结果提示姜黄油可能通过线粒体途径诱导肝癌细胞的凋亡。To evaluate the anti-human hepatocellular carcinoma activity of turmeric oil （TO）. Cell viability was assessed by MTT assay, cell apoptosis and mitochondrial membrane potential were measured by flow cytometry. The protein abundance of Bax, Bcl-2, caspase-3, caspase-9 and cytochrome C was analyzed by Western blot. The results demonstrated TO-induced apoptosis of Be1-7402 cells in a time- and dose- dependent manners. It was characterized by loss of mitochondrial membrane potential （△ψm） and enhanced Bax/Bcl-2 ratio. The release of cytochrome C from mitochondria and the activation of caspase-9 and -3 indicated that TO might induce apoptosis of Bel-7402 cells via mitochondrial-mediated pathway.

关 键 词：姜黄油 肝癌 凋亡 

分 类 号：R285.5[医药卫生—中药学]