Herein, novel ruthenium(II) complexes containing 1-methylimidazole as a ligand were obtained with the following formulas: [RuCl(1Meim)(dppb)(bpy)]Cl (1), [RuCl(1Meim)(dppb)(4,4′-DMbpy)]Cl (2), [RuCl(1Meim)(dppb)(5,5′-DMbpy)]Cl (3) and [RuCl(1Meim)(dppb)(phen)]Cl (4) where, 1Meim = 1-methylimidazole, dppb = 1,4-Bis(diphenylphosphino)butane, bpy = 2,2′-bipyridine, 4,4′-DMbpy = 4,4′-dimethyl-2,2′-bipyridine, 5,5′-DMbpy = 5,5′-dimethyl-2,2′-bipyridine and phen = 1,10-phenanthroline. Additionally, crystal structures containing the cations of (1) and (3) were obtained when the counter ion was exchanged, leading to the formation of [RuCl(1Meim)(dppb)(bpy)]PF₆ (5) and [RuCl(1Meim)(dppb)(5,5′-DMbpy)]PF₆ methanol solvate (6) where PF₆ = hexafluorophosphate, showing one 1-methylimidazole molecule coordinated through the imidazole nitrogen, as expected. The complexes were characterized by elemental analysis, molar conductivity, infrared and UV–Vis spectroscopy, ¹H, ¹³C{¹H} and ³¹P{¹H} NMR, mass spectrometry and cyclic voltammetry. The interactions of complexes 1–4 with DNA and human serum albumin (HSA) were evaluated, and the cytotoxicity profiles of compounds 1–4 were determined using four different tumor cell lines derived from human cancers (melanoma: HT-144, colon: HCT-8, breast: MDA-MB-231 and lung: A549). A higher cytotoxic activity was observed for compound (3) against non-small cell lung cancer (A549). Complex (3) inhibited the clonogenic capacity and cell cycle progression of A549 cells and induced apoptosis involving mitochondrial pathway activation. Therefore, the data obtained in the present study support further investigations concerning molecular targets of complex (3) in non-small cell lung cancer.

在此，以以下通式获得了含有1-甲基咪唑作为配体的新型钌（II）配合物：[RuCl（1Meim）（dppb）（bpy）] Cl（1），[RuCl（1Meim）（dppb）（4， 4'-DMbpy）] Cl（2），[RuCl（1Meim）（dppb）（5,5'-DMbpy）] Cl（3）和[RuCl（1Meim）（dppb）（phen）] Cl（4）其中，1Meim = 1-甲基咪唑，dppb = 1,4-双（二苯基膦基）丁烷，bpy = 2,2'-联吡啶，4,4'-DMbpy = 4,4'-二甲基-2,2'-联吡啶，5 ，5'-DMbpy = 5,5'-二甲基-2,2'-联吡啶和phen = 1,10-菲咯啉。此外，交换抗衡离子时，获得了包含（1）和（3）阳离子的晶体结构，从而形成了[RuCl（1Meim）（dppb）（bpy）] PF ₆（5）和[RuCl（1Meim）（dppb）（5,5'-DMbpy）] PF ₆甲醇溶剂化物（6），其中PF ₆  =六氟磷酸盐，显示一个1-甲基咪唑分子通过咪唑氮配位。通过元素分析，摩尔电导率，红外和UV-Vis光谱，¹ H，¹³ C { ¹ H}和³¹ P { ¹ H} NMR，质谱和循环伏安法对复合物进行表征。复合物的相互作用1 - 4与DNA和人血清白蛋白（HSA）进行评价，以及化合物的细胞毒性型材1 - 4使用源自人类癌症的四种不同的肿瘤细胞系（黑色素瘤：HT-144，结肠：HCT-8，乳腺癌：MDA-MB-231和肺：A549）确定肿瘤细胞株。观察到化合物（3）对非小细胞肺癌（A549）具有更高的细胞毒活性。复合物（3）抑制A549细胞的克隆能力和细胞周期进程，并诱导涉及线粒体途径活化的细胞凋亡。因此，本研究获得的数据支持有关非小细胞肺癌中复合物（3）的分子靶标的进一步研究。