Copper oxide nanoparticles aggravate airway inflammation and mucus production in asthmatic mice via MAPK signaling = 천식마우스의 점액분비를 촉진하는 구리산화물 나노파티클

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dc.contributor.authorJi Won Park-
dc.contributor.authorIn Chul Lee-
dc.contributor.authorNa Rae Shin-
dc.contributor.authorChan Mi Jeonn-
dc.contributor.authorOk-Kyoung Kwon-
dc.contributor.authorJ W Ko-
dc.contributor.authorJ C Kim-
dc.contributor.authorSei-Ryang Oh-
dc.contributor.authorI S Shin-
dc.contributor.authorKyung Seop Ahn-
dc.date.accessioned2017-04-19T10:18:46Z-
dc.date.available2017-04-19T10:18:46Z-
dc.date.issued2016-
dc.identifier.issn1743-5390-
dc.identifier.uri10.3109/17435390.2015.1078851ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/13169-
dc.description.abstractCopper oxide nanoparticles (CuONPs), metal oxide nanoparticles were used in multiple applications including wood preservation, antimicrobial textiles, catalysts for carbon monoxide oxidation and heat transfer fluid in machines. We investigated the effects of CuONPs on the respiratory system in Balb/c mice. In addition, to investigate the effects of CuONPs on asthma development, we used a murine model of ovalbumin (OVA)-induced asthma. CuONPs markedly increased airway hyper-responsiveness (AHR), inflammatory cell counts, proinflammatory cytokines and reactive oxygen species (ROS). CuONPs induced airway inflammation and mucus secretion with increases in phosphorylation of the MAPKs (Erk, JNK and p38). In the OVA-induced asthma model, CuONPs aggravated the increased AHR, inflammatory cell count, proinflammatory cytokines, ROS and immunoglobulin E induced by OVA exposure. In addition, CuONPs markedly increased inflammatory cell infiltration into the lung and mucus secretions, and MAPK phosphorylation was elevated compared to OVA-induced asthmatic mice. Taken together, CuONPs exhibited toxicity on the respiratory system, which was associated with the MAPK phosphorylation. In addition, CuONPs exposure aggravated the development of asthma. We conclude that CuONPs exposure has a potential toxicity in humans with respiratory disease.-
dc.publisherT&F (Taylor & Francis)-
dc.titleCopper oxide nanoparticles aggravate airway inflammation and mucus production in asthmatic mice via MAPK signaling = 천식마우스의 점액분비를 촉진하는 구리산화물 나노파티클-
dc.title.alternativeCopper oxide nanoparticles aggravate airway inflammation and mucus production in asthmatic mice via MAPK signaling-
dc.typeArticle-
dc.citation.titleNanotoxicology-
dc.citation.number4-
dc.citation.endPage452-
dc.citation.startPage445-
dc.citation.volume10-
dc.contributor.affiliatedAuthorJi Won Park-
dc.contributor.affiliatedAuthorIn Chul Lee-
dc.contributor.affiliatedAuthorNa Rae Shin-
dc.contributor.affiliatedAuthorChan Mi Jeonn-
dc.contributor.affiliatedAuthorOk-Kyoung Kwon-
dc.contributor.affiliatedAuthorSei-Ryang Oh-
dc.contributor.affiliatedAuthorKyung Seop Ahn-
dc.contributor.alternativeName박지원-
dc.contributor.alternativeName이인철-
dc.contributor.alternativeName신나래-
dc.contributor.alternativeName전찬미-
dc.contributor.alternativeName권옥경-
dc.contributor.alternativeName고제원-
dc.contributor.alternativeName김종춘-
dc.contributor.alternativeName오세량-
dc.contributor.alternativeName신인식-
dc.contributor.alternativeName안경섭-
dc.identifier.bibliographicCitationNanotoxicology, vol. 10, no. 4, pp. 445-452-
dc.identifier.doi10.3109/17435390.2015.1078851-
dc.subject.keywordAsthma-
dc.subject.keywordcopper oxide nanoparticle-
dc.subject.keywordMAPKs-
dc.subject.keywordrespiratory system-
dc.subject.localasthma-
dc.subject.localAsthma-
dc.subject.localcopper oxide nanoparticle-
dc.subject.localCopper oxide nanoparticle-
dc.subject.localCopper oxide nanoparticles-
dc.subject.localMAPK-
dc.subject.localMAPKs-
dc.subject.localrespiratory system-
dc.description.journalClassY-
Appears in Collections:
Jeonbuk Branch Institute > Functional Biomaterial Research Center > 1. Journal Articles
Ochang Branch Institute > Division of National Bio-Infrastructure > Bio-Resource Central Bank > 1. Journal Articles
Ochang Branch Institute > 1. Journal Articles
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
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