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氯化铈暴露导致小鼠海马损伤和炎症细胞因子表达改变。

Hippocampal damage and alterations of inflammatory cytokine expression in mice caused by exposure to cerium chloride.

机构信息

Medical College, Soochow University, Suzhou, 215123, China.

出版信息

Arch Environ Contam Toxicol. 2013 May;64(4):545-53. doi: 10.1007/s00244-012-9870-4. Epub 2013 Jan 22.

Abstract

Rare earth element (REE) exposure has been shown to induce central nerve system intoxication, but the molecular mechanisms by which this occurs are poorly understood. In this study, cerium (Ce), in the form of CeCl3, was administered by way of gavage to mice for 90 consecutive days, and cytokine expression, associated with neuroinflammation of hippocampus, as well as spatial memory were increased in mice. Significant Ce accumulation in hippocampus, which led to neuroinflammation and decreased spatial memory of mice, was observed. Furthermore, CeCl3 remarkably increased levels of Toll-like receptors 2 and 4, tumor necrosis factor-α, nucleic IκB kinase, factor-κB-inducible kinase, nucleic factor-κB, and p52 and p65 expression as well as significantly decreased levels of IκB and interleukin-2 expression. These results showed that neuroinflammation and damaged hippocampal function may be associated with CeCl3-induced neuerotoxicity. Our findings suggest the need for workers and consumers to exercise caution when handling REEs.

摘要

稀土元素(REE)暴露已被证明会导致中枢神经系统中毒,但发生这种情况的分子机制尚不清楚。在这项研究中,通过灌胃的方式向小鼠连续 90 天给予三氯化铈(CeCl3),结果显示与海马神经炎症相关的细胞因子表达以及空间记忆增加。观察到明显的 Ce 在海马中的积累,导致小鼠神经炎症和空间记忆下降。此外,CeCl3 显著增加了 Toll 样受体 2 和 4、肿瘤坏死因子-α、核酸 IκB 激酶、因子-κB 诱导激酶、核酸因子-κB、p52 和 p65 的表达,同时显著降低了 IκB 和白细胞介素-2 的表达。这些结果表明,神经炎症和海马功能受损可能与 CeCl3 诱导的神经毒性有关。我们的研究结果表明,工人和消费者在处理稀土元素时需要谨慎。

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