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Inhibitory effects of fucoidan on ICAM‐1 expression induced by inflammatory cytokine p53‐independent pathway in SH‐SY‐5Y
Author(s) -
Kang NamSung,
Jang KiHyo,
Kim MiHyun,
Lim Jung Dae,
Kang SeChan,
Sohn EunHwa
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.723.9
Subject(s) - fucoidan , icam 1 , inflammation , downregulation and upregulation , cytokine , proinflammatory cytokine , chemistry , nf κb , gene knockdown , cancer research , microbiology and biotechnology , cell adhesion molecule , biology , immunology , polysaccharide , gene , biochemistry
Fucoidans that are high‐molecular‐weight sulfated polysaccharides extracted from brown seaweeds have been known to have various biological activities. It is well known that the upregulation of adhesion molecules on endothelial cell surface is involved in inflammation responses, so we examined the effect of fucoidan on ICAM‐1 expression induced by inflammatory cytokines, f nTNF‐α combined with IFN‐γ in SH‐SY‐5Y cells. Both NO production and ICAM‐1 expression which were induced by inflammatory cytokines were decreased by treatment of fucoidan in SH‐SY‐5Y. We detected ICAM‐1 expression in same condition which was using p53 mutant SH‐SY‐5Y cells to investigate mechanisms involved in down regulation of ICAM‐1 expression. Because ICAM‐1 expression induced by inflammatory cytokines was not detected in p53 mutant SH‐SY‐5Y, we postulated p53 gene is necessary for induction of ICAM‐1 expression. But, decreasing effects of fucoidan on ICAM‐1 expression induced by inflammatory cytokines f nin SH‐SY‐5Y did not compare with decrease of p53 expression in dose‐dependent manners. From these results, we suggested that ICAM‐1 expression induced by inflammatory cytokines is decreased through p53 independent pathway by treatment of fucoidan in SH‐SY‐5Y. (This work was supported by grant No. RTI05‐01‐02 from the Regional Technology Innovation Program of the Ministry of Knowledge Economy(MKE))