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钌（II）-胸腺嘧啶配合物导致人早幼粒细胞白血病 HL-60 细胞生长抑制和半胱天冬酶介导的细胞凋亡诱导。

Ru(II)-Thymine Complex Causes Cell Growth Inhibition and Induction of Caspase-Mediated Apoptosis in Human Promyelocytic Leukemia HL-60 Cells.

机构信息

Gonçalo Moniz Institute, Oswaldo Cruz Foundation (IGM-FIOCRUZ/BA), Rua Waldemar Falcão, 121, Candeal, Salvador 40296-710, Bahia, Brazil.

Department of Chemistry, Federal University of Ouro Preto, Ouro Preto 35400-000, Minas Gerais, Brazil.

出版信息

Int J Mol Sci. 2018 May 30;19(6):1609. doi: 10.3390/ijms19061609.

DOI:10.3390/ijms19061609
PMID:29848969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6032384/
Abstract

Ruthenium-based compounds represent a class of potential antineoplastic drugs. Recently, we designed, synthesized, and identified the Ru(II)-thymine complex [Ru(PPh₃)₂(Thy)(bipy)]PF₆ (where PPh = triphenylphosphine, Thy = thymine and bipy = 2,2'-bipyridine) as a potent cytotoxic agent with the ability to bind to DNA and human and bovine serum albumins. In this study, the underlying cytotoxic mechanism of the [Ru(PPh₃)₂(Thy)(bipy)]PF₆ complex was assessed. This complex displayed potent cytotoxicity in different cancer cell lines; the morphology that is associated with apoptotic cell death, increased internucleosomal DNA fragmentation without cell membrane permeability, loss of the mitochondrial transmembrane potential, increased phosphatidylserine externalization, and caspase-3 activation were observed in human promyelocytic leukemia HL-60 cells that were treated with the complex. Moreover, pretreatment of HL-60 cells with Z-VAD(OMe)-FMK, a pan-caspase inhibitor, partially reduced the apoptosis that was induced by the complex, indicating that the apoptotic cell death occurred through a caspase-mediated pathway. In conclusion, the [Ru(PPh₃)₂(Thy)(bipy)]PF₆ complex displays potent cytotoxicity to different cancer cells and induces caspase-mediated apoptosis in HL-60 cells.

摘要

钌基化合物代表了一类有潜力的抗肿瘤药物。最近，我们设计、合成并鉴定了 Ru(II)-胸腺嘧啶配合物[Ru(PPh₃)₂(Thy)(bipy)]PF₆（其中 PPh = 三苯基膦，Thy = 胸腺嘧啶，bipy = 2,2'-联吡啶），它是一种具有结合 DNA 以及人和牛血清白蛋白能力的有效细胞毒性试剂。在这项研究中，我们评估了[Ru(PPh₃)₂(Thy)(bipy)]PF₆ 配合物的潜在细胞毒性机制。该配合物在不同的癌细胞系中表现出很强的细胞毒性；在人早幼粒细胞白血病 HL-60 细胞中观察到与凋亡细胞死亡相关的形态学变化，即出现核小体间 DNA 片段化增加而细胞膜通透性没有改变、线粒体跨膜电位丧失、磷脂酰丝氨酸外翻以及 caspase-3 激活。此外，HL-60 细胞用广谱 caspase 抑制剂 Z-VAD(OMe)-FMK 预处理后，部分减少了复合物诱导的凋亡，表明凋亡细胞死亡是通过 caspase 介导的途径发生的。总之，[Ru(PPh₃)₂(Thy)(bipy)]PF₆ 配合物对不同的癌细胞具有很强的细胞毒性，并诱导 HL-60 细胞中的 caspase 介导的凋亡。

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