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以联苯胺、4,4′-二氨基二苯醚和8-羟基喹啉为原料,合成了两个偶氮类配体BL1和BL2及由其桥联的与二氯·二联吡啶钌反应生成两个双核钌配合物1和2,通过核磁共振、红外光谱、质谱、元素分析等测试手段进行表征,并对配合物进行了电化学、细胞毒性及细胞周期的研究.结果表明:两个配合物对胶质瘤细胞(U251)均有明显的细胞毒性,半数抑制浓度IC50值分别为7.76和7.69μmol·L-1,配合物2对肺癌细胞(A549)和白血病细胞(K562)的细胞毒性约为配合物1细胞毒性的两倍;桥配体的刚柔性影响了配合物的结构,并因此影响了配合物对A549和K562的细胞毒性;配合物1与U251作用后,细胞周期阻滞在S期,而配合物2与U251作用后,细胞周期阻滞在G0/G1期.
Using benzidine, 4,4’-diaminodiphenyl ether and 8-hydroxyquinoline as raw materials, two azo ligands BL1 and BL2 and their bridged reaction with ruthenium dichloride dibipyridine Two binuclear ruthenium complexes 1 and 2 were synthesized and characterized by means of nuclear magnetic resonance, infrared spectroscopy, mass spectrometry and elemental analysis. The electrochemical, cytotoxicity and cell cycle studies of the complexes were carried out. The results showed that two The complexes showed obvious cytotoxicity on glioma cells (U251) with IC50 values of 7.76 and 7.69μmol·L-1, respectively. IC50 values of complexes 2 against lung cancer cells (A549) and leukemia cells (K562) Toxicity was about double the cytotoxicity of the complex 1; rigidity and flexibility of the bridge ligand affected the structure of the complex, and thus affected the cytotoxicity of the complex to A549 and K562; after the interaction between the complex 1 and U251, the cell cycle resistance Hysteresis in S phase, while the role of complex 2 and U251, cell cycle arrest in the G0 / G1 phase.