Abstract：
This study aimed to examine the immuntoxic effects of arsenic in the nervous system. Our results showed that arsenic increased corticocerebral and hippocampal weights (p < 0.05). Morris water maze tests revealed that arsenic significantly increased the time spent in latency to platform on the fourth day in 50 mg/L arsenic exposure and the fifth day in 25 and 50 mg/L arsenic exposure, as well as reduced the path length in target quadrant, time spent in target quadrant, and crossing times of the platform (p < 0.05). Hematoxylin-eosin staining showed that the vacuolated degeneration and pyknosis was found in the cerebral cortex and hippocampus of arsenic-treated mice. The mRNA levels of corticocerebral and hippocampal brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) were decreased in the 50 mg/L arsenic-treated group (p < 0.05). In addition, immunofluorescence staining showed that 25 and 50 mg/L arsenic all increased the expression of CD11b and glial fibrillary acidic protein (GFAP) in the cerebral cortex and hippocampus (p < 0.05). Arsenic markedly raised antigen-presenting molecule MHCII and CD40 mRNA levels in the cerebral cortex and hippocampus and upregulated the cell chemokine receptor 5 (CCR5) and CCR7 mRNA levels in the cerebral cortex at the 50 mg/L arsenic group, and increased the CCR7 mRNA levels in the hippocampus at the 25 and 50 mg/L arsenic groups (p < 0.05). Arsenic activated the nucleotide-binding domain-like receptor protein-3 (NLRP3) inflammasome, and enhanced its upstream promoter NF-κB protein level and downstream regulators IL-18 mRNA levels. Collectively, these results provide new evidences for the neuro-immune toxicity of arsenic.
摘要：
本研究旨在研究砷对神经系统的免疫毒性作用。我们的结果表明，砷增加皮质脑和海马的重量（p<0.05）。Morris水迷宫测试表明，砷在50mg/L砷暴露的第四天和25和50mg/L砷暴露的第五天显着增加了潜伏期到平台的时间。以及减少目标象限中的路径长度，在目标象限中花费的时间，和平台的穿越次数(p<0.05)。苏木精-伊红染色显示，在砷处理的小鼠的大脑皮层和海马中发现了空泡变性和固缩。50mg/L砷处理组脑皮质和海马脑源性神经营养因子（BDNF）和血管内皮生长因子（VEGF）的mRNA水平降低（p<0.05）。此外,免疫荧光染色显示，25和50mg/L砷均增加了大脑皮质和海马中CD11b和胶质纤维酸性蛋白（GFAP）的表达（p<0.05）。在50mg/L砷组中，砷显着提高了大脑皮层和海马中的抗原呈递分子MHCII和CD40mRNA水平，并上调了大脑皮层中的细胞趋化因子受体5（CCR5）和CCR7mRNA水平，25和50mg/L砷组海马CCR7mRNA水平升高（p<0.05）。砷激活核苷酸结合域样受体蛋白3（NLRP3）炎性体，并增强其上游启动子NF-κB蛋白水平和下游调节因子IL-18mRNA水平。总的来说，这些结果为砷的神经免疫毒性提供了新的证据。
