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45nm 银纳米粒子(AgNPs)对大鼠气管平滑肌的影响:一氧化氮的作用。

Effect of 45 nm silver nanoparticles (AgNPs) upon the smooth muscle of rat trachea: role of nitric oxide.

机构信息

Universidad Autónoma de San Luis Potosí, Facultad de Ciencias Químicas, San Luis Potosi, Mexico.

出版信息

Toxicol Lett. 2011 Dec 15;207(3):306-13. doi: 10.1016/j.toxlet.2011.09.024. Epub 2011 Oct 1.

DOI:10.1016/j.toxlet.2011.09.024
PMID:21983655
Abstract

AgNPs have been used to manufacture nanomaterials with new biophysical properties and functions. However, few experimental approaches have been used to assess their potential toxic or beneficial effects on human health, in association with the size, concentration, and biological target. The aim of this work was to evaluate the effects of the AgNPs on the smooth muscle of rat trachea. A single administration of AgNPs did not modify the smooth muscle tone, but, when the trachea rings were pre-treated with acetylcholine (ACh), AgNPs produced a contractile effect. Simultaneous administration of AgNPs and ACh resulted in a slight increase of smooth muscle contractility induced by ACh. AgNPs pretreatment followed by ACh administration showed that AgNPs exerted an important contraction effect induced by ACh after which muscle tone did not return to the basal level. This effect was associated with an increase in the production of nitric oxide (NO). The contractile response of the AgNPs induced by ACh was completely blocked when the rings were incubated, after the ACh but before the AgNPs administration, with 1400 W (NO blocker). The contractile effect was also abolished by atropine, which suggests that AgNPs alter ACh muscarinic receptor signaling. These data also show that AgNPs modify the contractile action of ACh through NO production and possibly induce hyper-reactivity of tracheal smooth muscle.

摘要

AgNPs 已被用于制造具有新的物理和生物学特性的纳米材料。然而,很少有实验方法被用来评估它们对人类健康的潜在毒性或有益影响,特别是与大小、浓度和生物靶标有关。本工作旨在评估 AgNPs 对大鼠气管平滑肌的影响。AgNPs 的单次给药不会改变平滑肌的张力,但当气管环用乙酰胆碱(ACh)预处理时,AgNPs 会产生收缩作用。AgNPs 与 ACh 同时给药会导致 ACh 引起的平滑肌收缩力略有增加。AgNPs 预处理后给予 ACh 显示,AgNPs 在 ACh 引起的收缩后发挥重要的收缩作用,此后肌肉张力不会恢复到基础水平。这种作用与一氧化氮(NO)的产生增加有关。当环在 ACh 给药后但在 AgNPs 给药前用 1400 W(NO 阻断剂)孵育时,AgNPs 诱导的 ACh 收缩反应完全被阻断。阿托品也能消除收缩作用,这表明 AgNPs 改变了 ACh 毒蕈碱受体信号。这些数据还表明,AgNPs 通过产生 NO 来改变 ACh 的收缩作用,并可能导致气管平滑肌的高反应性。

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