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首页> 外文期刊>Archives of Toxicology >Involvement of sensory nerves and TRPV1 receptors in the rat airway inflammatory response to two environment pollutants: diesel exhaust particles (DEP) and 1,2-naphthoquinone (1,2-NQ).
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Involvement of sensory nerves and TRPV1 receptors in the rat airway inflammatory response to two environment pollutants: diesel exhaust particles (DEP) and 1,2-naphthoquinone (1,2-NQ).

机译：感觉神经和TRPV1受体参与大鼠气道对两种环境污染物的炎症反应：柴油机尾气颗粒（DEP）和1,2-萘醌（1,2-NQ）。

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摘要

The environmental chemical 1,2-naphthoquinone (1,2-NQ) is implicated in the exacerbation of airways diseases induced by exposure to diesel exhaust particles (DEP), which involves a neurogenic-mediated mechanism. Plasma extravasation in trachea, main bronchus and lung was measured as the local (125)I-bovine albumin accumulation. RT-PCR quantification of TRPV1 and tachykinin (NK(1) and NK(2)) receptor gene expression were investigated in main bronchus. Intratracheal injection of DEP (1 and 5 mg/kg) or 1,2-NQ (35 and 100 nmol/kg) caused oedema in trachea and bronchus. 1,2-NQ markedly increased the DEP-induced responses in the rat airways in an additive rather than synergistic manner. This effect that was significantly reduced by L-732,138, an NK(1) receptor antagonist, and in a lesser extent by SR48968, an NK(2) antagonist. Neonatal capsaicin treatment also markedly reduced DEP and 1,2-NQ-induced oedema. Exposure to pollutants increased the TRPV1, NK(1) and NK(2) receptors gene expression in bronchus, an effect was partially suppressed by capsaicin treatment. In conclusion, our results are consistent with the hypothesis that DEP-induced airways oedema is highly influenced by increased ambient levels of 1,2-NQ and takes place by neurogenic mechanisms involving up-regulation of TRPV1 and tachykinin receptors.
机译：环境化学物质1,2-萘醌（1,2-NQ）与暴露于柴油机排气颗粒（DEP）引起的气道疾病加重有关，这涉及神经源性介导的机制。气管，主支气管和肺中的血浆外渗被测量为局部（125）I-牛白蛋白积累。 RT-PCR定量研究TRPV1和速激肽（NK（1）和NK（2））受体基因表达在主支气管中。气管内注射DEP（1和5 mg / kg）或1,2-NQ（35和100 nmol / kg）引起气管和支气管水肿。 1,2-NQ以加性而非协同的方式显着增加了DEP诱导的大鼠气道反应。 NK（1）受体拮抗剂L-732,138显着降低了该效应，而NK（2）拮抗剂SR48968则降低了这一作用。新生儿辣椒素治疗还显着降低DEP和1,2-NQ引起的水肿。接触污染物会增加支气管中TRPV1，NK（1）和NK（2）受体的基因表达，辣椒素处理可部分抑制这种作用。总之，我们的结果与以下假设相吻合：DEP诱导的气道水肿受1,2-NQ周围环境水平升高的高度影响，并通过涉及TRPV1和速激肽受体上调的神经发生机制发生。

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