Cao Shouying, Xie Yaqing, Lu Xiaotong, Zhao Zijie, Zhou Feiya, Wang Jie, Liang Lili
Department of Pharmaceutical Engineering, Anhui Provincial Key Laboratory of Tumor Evolution and Intelligent Diagnosis and Treatment, Bengbu Medical University, Bengbu 233030, PR China.
Department of Pharmaceutical Engineering, Anhui Provincial Key Laboratory of Tumor Evolution and Intelligent Diagnosis and Treatment, Bengbu Medical University, Bengbu 233030, PR China.
J Inorg Biochem. 2025 Apr;265:112832. doi: 10.1016/j.jinorgbio.2025.112832. Epub 2025 Jan 22.
Two Gd(III) complexes [GdL(HO)(NO)(CHOH)(CHCHOH)] (Gd1) and [Gd(OOCCH)L(HO)]•2(HO) (Gd2) (HL = 2-pyridylcarboxaldehyde isonicotinoylhydrazone) were synthesized with a Schiff base ligand. Crystallographic study reveals both Gd1 and Gd2 have a zero-dimensional mononuclear or binuclear structure. Magnetic investigations demonstrate that Gd1 and Gd2 exhibit potential magnetocaloric effects due to Gd(III) ions, which provide negligible magnetic anisotropy, and possess low-lying excited spin states. The antiproliferative activity of Gd1 and Gd2 to three tumor cell lines was conducted and the results showed Gd1 and Gd2 showed more pronounced antiproliferative activity to A549 cells better than cisplatin. The administration of Gd1 and Gd2 led to an increase in apoptosis among A549 cells in a concentration-dependent manner, along with a corresponding rise in the levels of reactive oxygen species (ROS) within the cells. Besides, Gd1 and Gd2 were able to significantly inhibit tumor cell migration. Cell cycle assay in A549 cells revealed that cell cycle was arrested of G0/G1 phase. Western blotting analysis showed that Gd1 and Gd2 complexes could promote apoptosis in A549 cells by modulating the expression of Bcl-2 and Bax proteins.
利用席夫碱配体合成了两种钆(III)配合物[GdL(HO)(NO)(CHOH)(CHCHOH)](Gd1)和[Gd(OOCCH)L(HO)]•2(HO)(Gd2)(HL = 2-吡啶甲醛异烟酰腙)。晶体学研究表明,Gd1和Gd2均具有零维单核或双核结构。磁性研究表明,由于钆(III)离子具有可忽略不计的磁各向异性且具有低激发自旋态,Gd1和Gd2表现出潜在的磁热效应。对Gd1和Gd2对三种肿瘤细胞系的抗增殖活性进行了研究,结果表明,Gd1和Gd2对A549细胞的抗增殖活性比顺铂更显著。Gd1和Gd2的给药导致A549细胞凋亡以浓度依赖性方式增加,同时细胞内活性氧(ROS)水平相应升高。此外,Gd1和Gd2能够显著抑制肿瘤细胞迁移。A549细胞的细胞周期分析表明细胞周期停滞在G0/G1期。蛋白质印迹分析表明,Gd1和Gd2配合物可通过调节Bcl-2和Bax蛋白的表达促进A549细胞凋亡。