To explore the relationship of oxidative stress and TGF-β 1/Smad3 pathway in the inhibition of osteoblast mineralization by copper chloride (CuCl₂), the osteoblasts were treated with CuCl₂ (0, 50 μM, 100 μM, 150 μM CuCl₂ 5H₂O) for 24 h. We found that Cu impaired the osteoblast structure, inhibited the glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities, alkaline phosphatase (ALP) content, mRNA expression of collagen I (COL-I), osteocalcin (OCN), insulin-like growth factor I (IGF-I), bone morphogenetic protein-2 (BMP-2), transforming growth factor β1 (TGF-β1) and core-binding factor α1 (Cbfα1), promoted the reactive oxygen species (ROS) production, inactivated the TGF-β1/Smad3 pathway. It indicates that the inactivated TGF-β1/Smad3 pathway leads to osteoblast impairment by CuCl₂. It will contribute to clarify the influence of CuCl₂ on the osteoblast mineralization.

为了探索氧化应激和TGF-β1 / Smad3途径在氯化铜（CuCl ₂）抑制成骨细胞矿化中的关系，分别用CuCl ₂（0，50μM，100μM，150μMCuCl ₂ 5H ）处理成骨细胞₂O）24小时。我们发现铜会破坏成骨细胞结构，抑制谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）活性，碱性磷酸酶（ALP）含量，胶原蛋白I（COL-1），骨钙蛋白（OCN），胰岛素的mRNA表达类生长因子I（IGF-1），骨形态发生蛋白2（BMP-2），转化生长因子β1（TGF-β1）和核心结合因子α1（Cbfα1）促进了活性氧（ROS）的产生，使TGF-β1/ Smad3通路失活。这表明灭活的TGF-β1/ Smad3途径导致CuCl ₂破坏成骨细胞。这将有助于阐明CuCl ₂对成骨细胞矿化的影响。