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目的合成钌配合物[Ru(MeIm)4(bpy)]2+并初步探讨其体外抗肝癌活性。方法利用元素分析、电喷雾质谱(ESI-MS)、核磁共振(NMR)等对目标化合物进行表征并通过溴化乙啶(EB)竞争结合实验检测其与DNA的结合能力;采用MTT法检测其对3株人肝癌细胞株HepG2、HCC-LM3和MHCC-97L细胞增殖的影响,用Hoechst33342染色法观察细胞凋亡的形态学改变,以流式细胞仪观察药物作用后细胞的凋亡率和细胞周期的变化。结果合成并表征了金属钌配合物[Ru(MeIm)4(bpy)]2+,同时竞争结合实验表明其能取代EB结合DNA。该化合物可抑制HepG2、HCC-LM3和MHCC-97L的增殖,呈浓度和时间依赖性。该化合物对HepG2细胞的增殖抑制作用最为明显,且浓度依赖性地诱导HepG2细胞凋亡,并随着作用时间的延长Sub-G1凋亡峰越增加。31.25～125μg/ml钌配合物阻滞细胞于G0/G1期,而浓度达250μg/ml时则阻滞细胞于G2/M期。结论合成的目标产物钌配合物[Ru(MeIm)4(bpy)]2+在体外可抑制人肝癌HepG2细胞的生长并能诱导其发生凋亡。
Aim To synthesize ruthenium complex [Ru (MeIm) 4 (bpy)] 2+ and investigate its anti-hepatoma activity in vitro. Methods The target compounds were characterized by elemental analysis, electrospray ionization mass spectrometry (ESI-MS) and nuclear magnetic resonance (NMR), and their binding ability to DNA was detected by competitive competition with ethidium bromide (EB) On the proliferation of three human hepatocellular carcinoma cell lines HepG2, HCC-LM3 and MHCC-97L cells. Morphological changes of apoptosis were observed by Hoechst33342 staining. The apoptotic rates of cells were observed by flow cytometry. Cycle changes. Results The Ru complex (Ru (MeIm) 4 (bpy)] 2+ was synthesized and characterized. The competitive binding assay indicated that it can replace EB-bound DNA. The compound inhibits the proliferation of HepG2, HCC-LM3 and MHCC-97L in a concentration and time-dependent manner. The compound has the most obvious inhibitory effect on the proliferation of HepG2 cells and induces the apoptosis of HepG2 cells in a concentration-dependent manner. The apoptosis peak of Sub-G1 increases with time. 31.25 ~ 125μg / ml ruthenium complex blocked cells in G0 / G1 phase, while the concentration of 250μg / ml blocked cells in G2 / M phase. Conclusion The target compound ruthenium complex [Ru (MeIm) 4 (bpy)] 2+ can inhibit the growth of HepG2 cells and induce its apoptosis in vitro.