中文摘要：

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.

英文摘要：

Two dinuclear ruthenium（ Ⅱ ） complexes 1 and 2 with two Ru（bpy）2 units （bpy= 2,2r-bipyridine） linked by azo ligands BL1 and BL2 which were synthesized from benzidine, 1, 4-diamido-diphenyl ether and 8- hydroxyquinoline were synthesized and characterized by 1H NMR, IR spectra, electrospray mass spectra and elemental analyses. Moreover, their electrochemical behavior, cytotoxic assays and cell cycle assays were studied. According to the studies, the two complexes were equally potent toward glioma cell （U251）, with the IC50 of 7. 76 and 7.69 μmol. L-1, respectively. However, the cytotoxicity of complex 2 doubled that of complex 1 on lung cancer cell （A549） and leukemia cell （K562）. The rigid BL1 and soft BL2 had an effect on the structure of the complexes 1 and 2, which suggested that the bridging ligands were responsible for the different cytotoxic activity between the two complexes on A549 and K562. Cell cycle analysis indicated that the complexes 1 and 2 caused U251 cell cycle arrested in S phase and GO/G1 phase, respectively.