Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo

Qingqing Chen, Yang Xue, Jiao SunShanghai Biomaterials Research and Testing Center, Shanghai Key Laboratory of Stomatology, Ninth People&#39;s Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People&#39;s Republic of ChinaAbstract: Silica nanoparticles (SiO2 NPs)...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Chen Q, Xue Y, Sun J
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2013
Materias:	Medicine (General) R5-920
Acceso en línea:	https://doaj.org/article/c35b11541ae5426295fd5357bf794913
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:c35b11541ae5426295fd5357bf794913
record_format	dspace
spelling	oai:doaj.org-article:c35b11541ae5426295fd5357bf7949132021-12-02T01:11:24ZKupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo1176-91141178-2013https://doaj.org/article/c35b11541ae5426295fd5357bf7949132013-03-01T00:00:00Zhttp://www.dovepress.com/kupffer-cell-mediated-hepatic-injury-induced-by-silica-nanoparticles-i-a12484https://doaj.org/toc/1176-9114https://doaj.org/toc/1178-2013Qingqing Chen, Yang Xue, Jiao SunShanghai Biomaterials Research and Testing Center, Shanghai Key Laboratory of Stomatology, Ninth People&#39;s Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People&#39;s Republic of ChinaAbstract: Silica nanoparticles (SiO2 NPs) have been shown to exert cytotoxic effects in hepatocytes and to cause liver injury. In the liver, Kupffer cells (KCs), as the resident macrophages, play an important role in the normal physiology and homeostasis of the liver. Nevertheless, few studies have attempted to clarify the role of KCs in hepatic injury induced by SiO2 NPs. In this study, we treated Buffalo rat liver (BRL) cells with the supernatants of SiO2 NP-stimulated KCs to determine KC-mediated hepatotoxicity and its underlying preliminary mechanism. We also examined the response of KCs and liver injury in vivo after the administration of SiO2 NPs. The results showed that KCs stimulated by SiO2 NPs release large amounts of reactive oxygen species, tumor necrosis factor-a and nitric oxide. After BRL cells were cultured with the supernatants of SiO2 NP-stimulated KCs, the viability of BRL cells was reduced, and increases in aspartate aminotransferase and lactate dehydrogenase leakage were observed. Exposure to SiO2 NPs in vivo caused KC hyperplasia, hepatic inflammation, and oxidative stress, which led to changes in the biochemical composition of the liver. These data suggest that SiO2 NPs activate KCs to mediate hepatic injury and that the preliminary mechanism involves the release of bioactive substances from KCs.Keywords: silica nanoparticles, Kupffer cells, coculture, oxidative stress, metabolomics, hepatic injuryChen QXue YSun JDove Medical PressarticleMedicine (General)R5-920ENInternational Journal of Nanomedicine, Vol 2013, Iss default, Pp 1129-1140 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine (General) R5-920
spellingShingle	Medicine (General) R5-920 Chen Q Xue Y Sun J Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
description	Qingqing Chen, Yang Xue, Jiao SunShanghai Biomaterials Research and Testing Center, Shanghai Key Laboratory of Stomatology, Ninth People&#39;s Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People&#39;s Republic of ChinaAbstract: Silica nanoparticles (SiO2 NPs) have been shown to exert cytotoxic effects in hepatocytes and to cause liver injury. In the liver, Kupffer cells (KCs), as the resident macrophages, play an important role in the normal physiology and homeostasis of the liver. Nevertheless, few studies have attempted to clarify the role of KCs in hepatic injury induced by SiO2 NPs. In this study, we treated Buffalo rat liver (BRL) cells with the supernatants of SiO2 NP-stimulated KCs to determine KC-mediated hepatotoxicity and its underlying preliminary mechanism. We also examined the response of KCs and liver injury in vivo after the administration of SiO2 NPs. The results showed that KCs stimulated by SiO2 NPs release large amounts of reactive oxygen species, tumor necrosis factor-a and nitric oxide. After BRL cells were cultured with the supernatants of SiO2 NP-stimulated KCs, the viability of BRL cells was reduced, and increases in aspartate aminotransferase and lactate dehydrogenase leakage were observed. Exposure to SiO2 NPs in vivo caused KC hyperplasia, hepatic inflammation, and oxidative stress, which led to changes in the biochemical composition of the liver. These data suggest that SiO2 NPs activate KCs to mediate hepatic injury and that the preliminary mechanism involves the release of bioactive substances from KCs.Keywords: silica nanoparticles, Kupffer cells, coculture, oxidative stress, metabolomics, hepatic injury
format	article
author	Chen Q Xue Y Sun J
author_facet	Chen Q Xue Y Sun J
author_sort	Chen Q
title	Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
title_short	Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
title_full	Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
title_fullStr	Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
title_full_unstemmed	Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
title_sort	kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo
publisher	Dove Medical Press
publishDate	2013
url	https://doaj.org/article/c35b11541ae5426295fd5357bf794913
work_keys_str_mv	AT chenq kupffercellmediatedhepaticinjuryinducedbysilicananoparticlesinvitroandinvivo AT xuey kupffercellmediatedhepaticinjuryinducedbysilicananoparticlesinvitroandinvivo AT sunj kupffercellmediatedhepaticinjuryinducedbysilicananoparticlesinvitroandinvivo
_version_	1718403282591809536

Kupffer cell-mediated hepatic injury induced by silica nanoparticles in vitro and in vivo

Ejemplares similares