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首页> 外文期刊>Journal of applied toxicology >Fetal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin induces expression of the chemokine genes Cxcl4 and Cxcl7 in the perinatal mouse brain.
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Fetal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin induces expression of the chemokine genes Cxcl4 and Cxcl7 in the perinatal mouse brain.

机译：胎儿暴露于2,3,7,8-四氯二苯并-p-二恶英会诱导围生期小鼠脑中趋化因子基因Cxcl4和Cxcl7的表达。

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摘要

Fetal exposure to dioxins affects brain development and influences behaviors in human and laboratory animals. However, the cellular target and mechanisms of the neurotoxic action of dioxins are largely unknown. To investigate the molecular basis for the neurotoxicity of dioxins, pregnant C57BL/6 mice were exposed to 5 microg kg(-1) body weight of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by a single gavage on gestational day 12.5 (GD 12.5), and gene expression of the whole fetal brain at GD 18.5 was profiled by DNA microarray analysis. The analysis revealed that the expression of two chemokine genes, Cxcl4 and Cxcl7, was up-regulated by TCDD exposure. Real-time PCR analysis verified that they were up-regulated by TCDD in both male and female brains, while the mRNA levels of a majority of other chemokines and their receptor genes were not affected. The up-regulation was TCDD dose-dependent and peaked at GD 15.5-18.5. In situ hybridization analysis showed that the Cxcl4 mRNA expression was localized in part of the surface of cerebral cortex and that the level was increased by TCDD treatment. These results suggest that Cxcl4 and Cxcl7 play a role in the development of neurobehavioral alterations that are triggered by in utero TCDD exposure and later surface in adults.
机译：胎儿暴露于二恶英会影响大脑发育并影响人类和实验动物的行为。但是，二恶英的细胞靶标和神经毒性作用的机制尚不清楚。若要调查二恶英的神经毒性的分子基础，怀孕的C57BL / 6小鼠暴露于5微克kg（-1）体重的2,3,7,8-四氯二苯并-p-二恶英（TCDD），妊娠第12.5天（GD 12.5），整个胎儿大脑的基因表达为GD 18.5，通过DNA微阵列分析进行分析。分析显示，TCDD暴露可上调两个趋化因子基因Cxcl4和Cxcl7的表达。实时PCR分析证实，TCDD在雄性和雌性大脑中均上调了它们，而其他大多数趋化因子的mRNA水平及其受体基因均未受到影响。上调是TCDD剂量依赖性的，并在GD 15.5-18.5达到峰值。原位杂交分析表明，Cxcl4 mRNA表达局限于大脑皮层表面的一部分，并且通过TCDD处理可提高该水平。这些结果表明，Cxcl4和Cxcl7在子宫内TCDD暴露和成人随后的表面触发的神经行为改变的发生中起作用。

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