双去甲氧基姜黄素通过降低线粒体膜电位诱导人白血病K562细胞凋亡  

Bisdemethoxycurcumin Induced Human Leukemia K562 Cells Apoptosis Through Down-regulation of Mitochondrial Membrane Potential

作　　者：苗久旺[1,2] 张钦德[2] 王洪波[3] 傅风华[1,3] 

机构地区：[1]山东中医药大学药学院,济南250355 [2]山东中医药高等专科学校,山东烟台264199 [3]烟台大学药学院,山东烟台264003

出　　处：《中国实验方剂学杂志》2015年第24期109-113,共5页Chinese Journal of Experimental Traditional Medical Formulae

基　　金：山东省中医药科技发展计划项目(2011-151)

摘　　要：目的:探讨双去甲氧基姜黄素对K562细胞增殖的影响及其机制。方法:以1,10,30,50,100μmol·L^(^(-1))的双去甲氧基姜黄素对K562细胞作用48 h或72 h后MTT法检测细胞增殖;以10,30,50μmol·L^(-1)的双去甲氧基姜黄素对K562细胞作用24 h或48 h实验,另设空白组,AO/EB双染法倒置荧光显微镜观察凋亡形态,Rh123染色流式细胞仪检测线粒体膜电位,Annxin V/PI染色流式细胞仪检测凋亡率,Westren blot方法检测Bcl-2,Bax的表达活性。结果:与空白组比较,双去甲氧基姜黄素可剂量依赖性抑制K562细胞的增殖,在30,50μmol·L^(-1)浓度下,双去甲氧基姜黄素可诱导细胞凋亡,下调Bcl-2/Bax,并可降低线粒体的膜电位(P<0.01)。结论:双去甲氧基姜黄素可抑制K562细胞的增殖,作用机制可能与改变线粒体膜电位诱导的细胞凋亡有关。Objective： To explore the antitumor effects and mechanisms of bisdemethoxycurcumin（ BDMC） on K562 cells. Method： K562 cells were treated with 1,10,30,50,100 μmol·L-1of BDMC for 48 h or 72 h,then the anti-proliferative effect was assessed by MTT assay. K562 cells were treated with 10,30,50μmol·L-1of BDMC for 24 h or 48 h,and another blank group was also established. The apoptosis morphology was observed by AO / EB staining using fluorescence microscope,mitochondrial membrane potential（ MMP） was detected by Rhodamine 123 staining using flow cytometry instrument and apoptosis rate was detected by Annexin V /PI staining using flow cytometry instrument. The expression of Bcl-2,Bax was evaluated by Western blot method.Result： BDMC could inhibit the proliferation of K562 cells in a dose dependent manner when compared with the blank group. BDMC at the dose of 30,50 μmol·L-1could induce cell apoptosis,decrease the ratio of Bcl-2 / Bax and reduce mitochondrial membrane potential. Conclusion： BDMC could inhibit proliferation of K562 cells,and its mechanism may be related with the induction of cell apoptosis via mitochondria pathway.

关 键 词：双去甲氧基姜黄素 抗肿瘤 凋亡 线粒体膜电位 

分 类 号：R285.5[医药卫生—中药学]