2005 Fiscal Year Final Research Report Summary
Study of the treatment on an immune-mediated liver injury by the high molecular weight hyaluronan.
| Project/Area Number |
15590613
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Obihiro University of Agriculture and Veterinary Medicine (2005)
Asahikawa Medical College (2003-2004) |
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Principal Investigator |
NAKAMURA Kimihide Obihiro University of Agriculture and Veterinary Medicine, Department of Agriculture, Professor, 畜産学部, 教授 (20217839)
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| Project Period (FY) |
2003 – 2005
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| Keywords | Concanavalin A / Immune-mediated liver injury / Cytokine / Chemokine / High molecular weight hyaluronan / Polysaccharide / Fucoidan / Immune tolerance |
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| Research Abstract |
1.Concanavalin A (Con A) induced more severe liver injury and release of TNF-α and IFN-γ in female mice compared with male mice.
2.Macrophage inflammatory protein-1α is produced from Kupffer cells after Con A injection, and this CC chemokine plays a crucial role in Con A-induced liver injury through induction of proinflammatory cytokines (TNF-α and IFN-γ) in mice.
3.High, but not low, molecular weight hyaluronan prevents liver injury by redusing proinflammatory cytokines (TNF-α and IFN-γ) in Con A-induced liver injury model.
4.Fucoidan is a complex of sulfated polysaccharides derived from non-mammalian origin such as marine brown algae. Fucoidan prevents Con A-induced liver injury by mediating the endogenous IL-10 production and the inhibition of proinflammatory cytokines (TNF-α and IFN-γ) in mice, and that fucoidan induced the IL-10 production from Kupffer cells through a macrophage scavenger receptor in mice.
5.The repeated administrations of Con A elicited Th1 to Th2 cytokine shift and the tolerant state against the Con A-induced liver injury in mice.
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