| Registro completo |
| Provedor de dados: |
OAK
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| País: |
Japan
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| Título: |
Fucoidan prevents concanavalin A-induced liver injury through induction of endogenous IL-10 in mice
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| Autores: |
Saito, Ako
Yoneda, Masashi
Yokohama, Shiro
Okada, Mitsuyoshi
Haneda, Masakazu
Nakamura, Kimihide
中村, 公英
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| Data: |
2006-07
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| Ano: |
2006
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| Palavras-chave: |
Concanavalin A
Fucoidan
Liver injury
Cytokine
Kupffer cell
Scavenger receptor
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| Resumo: |
Fucoidan is a complex of sulfated polysaccharides derived from non-mammalian origin such as marine brown algae and induces cytokine expression. We investigated the effect of fucoidan on concanavalin A (Con A)-induced liver injury in mice. Liver injury was induced by an intravenous injection of Con A (18.5 mg/kg). Various doses of fucoidan (1-30 mg/kg) were intravenously administered 30 min before Con A injection. The plasma alanine aminotransferase (ALT) and several cytokines levels were determined, and hepatic histological changes were also assessed. The effect of fucoidan administration by itself on induction of interleukin (IL)-10 in plasma and liver tissue was investigated. Con A administration induced an elevation of plasma ALT level, and fucoidan administration dose-dependently prevented the Con A-induced elevation of plasma ALT. Con A administration increased plasma TNF-alpha and IFN-gamma levels, and fucoidan pretreatment significantly inhibited these alterations and increased plasma IL-10 level. The inhibitory effect of fucoidan on Con A-induced liver injury and production of proinflammatory cytokines were reversed by anti-mouse IL-10 antibody pretreatment. Fucoidan induced the IL-10 production in plasma and liver tissue. These findings suggest that fucoidan prevents Con A-induced liver injury by mediating the endogenous IL-10 production and the inhibition of proinflammatory cytokine in mice. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
http://www.sciencedirect.com/science/journal/13866346
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| Idioma: |
Inglês
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| Identificador: |
http://ir.obihiro.ac.jp/dspace/handle/10322/66
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| Editor: |
ELSEVIER
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| Formato: |
application/pdf
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