Three Ru(II)-DMSO complexes (1-3) containing 2-(3-pyrazolyl)pyridine (PzPy), 2-pyrazol-3-ylfuran (PzO), or 2-pyrazol-3-ylthiophene (PzS) ligand, were synthesized and characterized. The monodentate coordination of the heterocyclic pyrazolyl ligand (Pz^Py) with Ru(II) ion via N atom was confirmed by single crystal X-ray diffraction. Complex 1 could be converted to the known η²-bidentate Pz^Py complex cis(Cl), cis(S)-[RuCl₂(Pz^Py)(DMSO)₂] (4) under reflux conditions. The mechanism underlying binding mode transformation was studied by ¹H NMR spectroscopy and density functional theory (DFT) calculations. The binding abilities of the complexes (1–4) with calf-thymus (CT) DNA and bovine serum albumin (BSA) were investigated using spectroscopic and molecular docking techniques. Among the four Ru(II) complexes, complexes 1 and 3 inhibited the long-term proliferation of human breast cancer cells, whereas complexes 2 and 4 did not inhibit their proliferation to a considerable extent. Interestingly, complexes 1 and 3 did not induce significant cell death but rather attenuated the clonogenicity of breast cancer cells by upregulating reactive oxygen species (ROS), endoplasmic reticulum (ER) and autophagic stress.

三个含有 2-(3-吡唑基)吡啶 (PzPy)、2-吡唑-3-基呋喃 (PzO) 或 2-吡唑-3-基噻吩 (PzS) 配体的 Ru(II)-DMSO 配合物 (1-3)，进行了合成和表征。通过单晶 X 射线衍射证实了杂环吡唑基配体 (Pz ^Py ) 与 Ru(II) 离子通过N 原子的单齿配位。配合物1可以转化为已知的η ² -二齿 Pz ^Py配合物cis (Cl), cis ( S )-[RuCl ₂ (Pz ^Py )(DMSO) ₂ ] ( 4) 在回流条件下。^通过1 H NMR 光谱和密度泛函理论 (DFT) 计算研究了结合模式转变的机制。使用光谱和分子对接技术研究了复合物 ( 1-4 )与小牛胸腺 (CT) DNA 和牛血清白蛋白 (BSA) 的结合能力。在四种 Ru(II) 配合物中，配合物1和3对人乳腺癌细胞的长期增殖有抑制作用，而配合物2和4对它们的增殖没有明显抑制作用。有趣的是，配合物1和3没有诱导显着的细胞死亡，而是通过上调活性氧（ROS）、内质网（ER）和自噬应激来减弱乳腺癌细胞的克隆形成。