College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China.
School of Medicine, Tongren Polytechni College, Guizhou 554300, China.
Int J Mol Sci. 2019 Mar 22;20(6):1469. doi: 10.3390/ijms20061469.
Research has shown that nano-copper (nano-Cu) can cause damage to the spleen and immune system yet their mechanisms of cytotoxicity are poorly understood. Our aim is to explore the potential immunotoxicity in the spleen of rats after nano-Cu exposure. The results of hematologic parameters, lymphocyte subsets, immunoglobulins, and histopathology indicated that copper obviously changed the immune function of the spleen. The levels of antioxidants (SOD, CAT, GSH-Px), oxidants (iNOS, NO, MDA), and anti-oxidative signalling pathway of Nrf2 (Nrf2 and HO-1) were strongly induced by nano-Cu. The expression of mRNA and protein of pro-/anti-inflammatory (IFN-γ, TNF-α, MIP-1α, MCP-1, MIF, IL-1/-2/-4/-6) cytokines were increased by nano-Cu. The expression of regulatory signal pathways, MAPKs and PI3-K/Akt were activated, which might be involved in the inflammatory responses and immunomodulatory processes of sub-acute nano-Cu exposure. The immune function of the spleen was repressed by nano-Cu induced oxidative stress and inflammation.
研究表明,纳米铜(nano-Cu)会对脾脏和免疫系统造成损害,但它们的细胞毒性机制尚不清楚。我们的目的是探索纳米铜暴露后大鼠脾脏的潜在免疫毒性。血液学参数、淋巴细胞亚群、免疫球蛋白和组织病理学的结果表明,铜明显改变了脾脏的免疫功能。抗氧化剂(SOD、CAT、GSH-Px)、氧化剂(iNOS、NO、MDA)和 Nrf2 的抗氧化信号通路(Nrf2 和 HO-1)的水平被纳米铜强烈诱导。促炎/抗炎(IFN-γ、TNF-α、MIP-1α、MCP-1、MIF、IL-1/-2/-4/-6)细胞因子的 mRNA 和蛋白表达被纳米铜增加。调节信号通路 MAPKs 和 PI3-K/Akt 的表达被激活,这可能涉及亚急性纳米铜暴露的炎症反应和免疫调节过程。纳米铜诱导的氧化应激和炎症抑制了脾脏的免疫功能。