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Fucoidan prevents concanavalin A-induced liver injury through induction of endogenous IL-10 in mice
- Source :
-
Hepatology Research . Jul2006, Vol. 35 Issue 3, p190-198. 9p. - Publication Year :
- 2006
-
Abstract
- Abstract: 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 (18.5mg/kg). Various doses of fucoidan (1–30mg/kg) were intravenously administered 30min 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-α and IFN-γ 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. [Copyright &y& Elsevier]
- Subjects :
- *POLYSACCHARIDES
*CYTOKINES
*GENE expression
*INTERLEUKIN-10
*TUMOR necrosis factors
Subjects
Details
- Language :
- English
- ISSN :
- 13866346
- Volume :
- 35
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- Hepatology Research
- Publication Type :
- Academic Journal
- Accession number :
- 21577965
- Full Text :
- https://doi.org/10.1016/j.hepres.2006.03.012