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.
出处
《中国实验方剂学杂志》
CAS
CSCD
北大核心
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)
关键词
双去甲氧基姜黄素
抗肿瘤
凋亡
线粒体膜电位
bisdemethoxycurcumin
antitumor
apoptosis
mitochondrial membrane potential
