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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 investigate the effect of didemethoxy curcumin on the proliferation of K562 cells and its mechanism. METHODS: K562 cells were treated with 1, 10, 30, 50, 100μmol·L ~ (-1) dithiodoxy curcumin for 48 h or 72 h and MTT assay was used to detect cell proliferation. Double demethoxy curcumin treated with 50μmol·L -1 for 24 h or 48 h, K562 cells were also treated with blank group. AO / EB double staining was used to observe the morphological changes of apoptotic cells. Rh123 staining flow cytometry Mitochondrial membrane potential was detected by cytometry. The apoptosis rate was detected by Annxin V / PI staining flow cytometry. The expression of Bcl-2 and Bax was detected by Westren blot. RESULTS: Compared with the blank group, didemethoxy curcumin could inhibit the proliferation of K562 cells in a dose-dependent manner. At the concentrations of 30 and 50 μmol·L -1, didemethoxy curcumin induced cell apoptosis , Down-regulated Bcl-2 / Bax and decreased mitochondrial membrane potential (P <0.01). CONCLUSION: Didemethoxy curcumin can inhibit the proliferation of K562 cells. The mechanism may be related to the change of mitochondrial membrane potential-induced apoptosis.