College of Animal Science, Anhui Science and Technology University, Fengyang, 233100, China; Anhui Province Key Laboratory of Animal Nutritional Regulation and Health, Anhui Science and Technology University, Fengyang, 233100, China.
Animal Health Quarantine Station of Daqing Agricultural and Rural Bureau, Daqing, 163000, China.
Environ Toxicol Pharmacol. 2021 May;84:103613. doi: 10.1016/j.etap.2021.103613. Epub 2021 Feb 8.
To explore the relationship of oxidative stress and TGF-β 1/Smad3 pathway in the inhibition of osteoblast mineralization by copper chloride (CuCl), the osteoblasts were treated with CuCl (0, 50 μM, 100 μM, 150 μM CuCl 5HO) 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 CuCl. It will contribute to clarify the influence of CuCl on the osteoblast mineralization.
为了探讨氯化铜（CuCl）抑制成骨细胞矿化过程中氧化应激与 TGF-β1/Smad3 通路的关系，将成骨细胞用 CuCl（0、50 μM、100 μM、150 μM CuCl·5H2O）处理 24 h。结果发现，Cu 破坏了成骨细胞的结构，抑制了谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）的活性、碱性磷酸酶（ALP）的含量、Ⅰ型胶原（COL-I）、骨钙素（OCN）、胰岛素样生长因子 I（IGF-I）、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）的 mRNA 表达，促进了活性氧（ROS）的产生，使 TGF-β1/Smad3 通路失活。这表明 CuCl 通过使 TGF-β1/Smad3 通路失活导致成骨细胞损伤。这将有助于阐明 CuCl 对成骨细胞矿化的影响。
