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首页> 外文期刊>Journal of Hazardous Materials >Cardiac inflammation involving in PKC epsilon or ERK1/2-activated NF-kappa B signalling pathway in mice following exposure to titanium dioxide nanoparticles
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Cardiac inflammation involving in PKC epsilon or ERK1/2-activated NF-kappa B signalling pathway in mice following exposure to titanium dioxide nanoparticles

机译：暴露于二氧化钛纳米颗粒后，小鼠的心脏炎症涉及PKC epsilon或ERK1 / 2激活的NF-κB信号通路

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摘要

The evaluation of toxicological effects of nanoparticles (NPs) is increasingly important due to their growing occupational use and presence as compounds in consumer products. Recent researches have demonstrated that long-term exposure to air particulate matter can induce cardiovascular events, but whether cardiovascular disease, such as cardiac damage, is induced by NP exposure and its toxic mechanisms is rarely evaluated. In the present study, when mice were continuously exposed to TiO2 NPs at 2.5, 5 or 10 mg/kg BW by intragastric administration for 90 days, obvious histopathological changes, and great alterations of NF-kappa B and its inhibitor I-kappa B, as well as TNF-alpha, IL-beta, IL-6 and IFN-alpha expression were induced. The NPs significantly decreased Ca2+-ATPase, Ca2+/Mg2+-ATPase and Na+/K+-ATPase activities and enhanced NCX-1 content. The NPs also considerably increased CAMK II and alpha 1/beta 1-AR expression and up-regulated p-PKC epsilon and p-ERIC1/2 in a dose-dependent manner in the mouse heart. These data suggest that low-dose and long-term exposure to TiO2 NPs may cause cardiac damage such as cardiac fragmentation or disordered myocardial fibre arrangement, tissue necrosis, myocardial haemorrhage, swelling or cardiomyocyte hypertrophy, and the inflammatory, response was potentially mediated by NF-kappa B activation via the PKC epsilon or ERK1/2 signalling cascades in mice. (C) 2016 Published by Elsevier B.V.
机译：由于纳米颗粒（NPs）在职业中的用途日益广泛以及在消费品中以化合物的形式存在，因此对其毒理作用的评估变得越来越重要。最近的研究表明，长期暴露于空气颗粒物会诱发心血管事件，但是NP暴露是否会诱发心血管疾病（例如心脏损害），并且很少评估其毒性机制。在本研究中，当通过胃内给药连续90天使小鼠连续暴露于2.5、5或10 mg / kg BW的TiO2 NPs时，明显的组织病理学变化以及NF-κB及其抑制剂I-κB的巨大变化，以及TNF-α，IL-β，IL-6和IFN-α表达被诱导。 NPs显着降低Ca2 + -ATPase，Ca2 + / Mg2 + -ATPase和Na + / K + -ATPase活性，并增加NCX-1含量。在小鼠心脏中，NP也以剂量依赖的方式大大增加了CAMK II和α1 /β1-AR的表达，并上调了p-PKC epsilon和p-ERIC1 / 2。这些数据表明，低剂量和长期暴露于TiO2 NPs可能会导致心脏损害，例如心脏破碎或心肌纤维排列紊乱，组织坏死，心肌出血，肿胀或心肌细胞肥大，而炎症反应可能是由NF介导的。小鼠中通过PKC epsilon或ERK1 / 2信号级联反应激活KappaB。 （C）2016由Elsevier B.V.发布

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  • 来源
    《Journal of Hazardous Materials》 |2016年第5期|68-77|共10页
  • 作者

    Yu Xiaohong; Hong Fashui; Zhang Yu-Qing;

  • 作者单位

    Soochow Univ, Sch Basic Med & Biol Sci, Dept Appl Biol, RM 702-2303,Renai Rd 199, Suzhou 215123, Peoples R China;

    Huaiyin Normal Univ, Jiangsu Collaborat Innovat Ctr Reg Modern Agr & E, Huaian 223300, Peoples R China|Huaiyin Normal Univ, Jiangsu Key Lab Ecoagr Biotechnol Hongze Lake, Huaian 223300, Peoples R China;

    Soochow Univ, Sch Basic Med & Biol Sci, Dept Appl Biol, RM 702-2303,Renai Rd 199, Suzhou 215123, Peoples R China;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Titanium dioxide nanoparticles; Mice; Cardiac damage; Inflammatory response; Molecular mechanisms;

    机译：二氧化钛纳米粒子;小鼠;心脏损伤;炎症反应;分子机制;

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