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研究新合成的一氧化氮供体——核苷衍生物6-甲基-4-(2-氟-3,5-二-O-苯甲酰基-1-β-D-呋喃阿拉伯糖)-[1,2,5]噁二唑[3,4-d]嘧啶-5(4H),7(6H)-二酮1-氧化物(MOPDO)抑制人肝癌细胞HepG2增殖、诱导凋亡的作用。以不同浓度的MOPDO作用于人肝癌细胞HepG2,MTT检测与相差显微镜观察相结合,分析MOPDO对HepG2细胞增殖的影响;膜联蛋白-V/PI双染检测细胞凋亡率;JC-1染色检测线粒体膜电位(?ψm)变化;硝酸酶法测定细胞培养液中NO的含量。结果发现,MOPDO以时间和剂量依赖性方式抑制HepG2细胞的增殖,细胞形态出现相应的变化;细胞凋亡率的增加呈时-效和量-效关系;JC-1染色显示,线粒体膜电位随着MOPDO剂量的增加降低;MOPDO释放的NO量呈剂量依赖性增加。表明线粒体可能参与介导MOPDO抑制HepG2细胞的增殖、诱导其凋亡的作用。
A new synthetic nitric oxide donor-nucleoside derivative, 6-methyl-4- (2-fluoro-3,5-di-O-benzoyl-1-β-D-arabinofuranosyl) Effect of [1,2,5] oxadiazole [3,4-d] pyrimidine-5 (4H), 7 (6H) -dione 1-oxide (MOPDO) on Proliferation and Induction of Apoptosis in Human Hepatoma HepG2 Cells . The effect of MOPDO on the proliferation of HepG2 cells was analyzed by MTT assay and phase contrast microscopy. The apoptotic rate of HepG2 cells was detected by Annexin-V / PI double staining. The expression of JC-1 was detected by MTT assay Mitochondrial membrane potential (? Ψm) changes; nitric acid method for determination of cell culture medium NO content. The results showed that MOPDO inhibited the proliferation of HepG2 cells in a time and dose-dependent manner, with corresponding changes of cell morphology. The increase of apoptosis rate showed a time-effect and dose-effect relationship. The expression of JC-1 showed that the mitochondrial membrane potential The increase of MOPDO dose decreased; the amount of NO released by MOPDO increased in a dose-dependent manner. Indicating that mitochondria may be involved in mediating MOPDO inhibit HepG2 cell proliferation and induce apoptosis.