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Fucoidan inhibits the expression iNOS induced by TNF‐α and IFN‐γ in C6 glioma cells; Regulation by p38 MAPK, AP‐1, IRF‐1 and scavenger receptor B1
Author(s) -
Kang Nam Sung,
Do Hang Thi Thu,
Jang SeonA,
Pyo Suhkneung,
Sohn Eun Hwa
Publication year - 2009
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.23.1_supplement.739.20
Subject(s) - fucoidan , mapk/erk pathway , p38 mitogen activated protein kinases , chemistry , tumor necrosis factor alpha , microbiology and biotechnology , pharmacology , biology , signal transduction , biochemistry , immunology , polysaccharide
In neurodegenerative disorders activated glial cells overproduce NO and iNOS, which causes neurotoxicity. Here, we examined the action of fucoidan on TNF‐α and IFN‐γ(T/I‐) induced NO production in C6 cells. Fucoidan suppressed T/I‐induced NO production and iNOS expression. In addition, fucoidan inhibited T/I‐induced AP‐1, IRF‐1, and p38 MAPK activation and induced SR‐B1 expression. Blocking of SR‐B1 didn't reverse the inhibitory effect of fucoidan on T/I‐ stimulated NO production. However, inhibition of SR‐B1 expression by siRNA increased iNOS expression and p38‐p in T/I‐stimulated C6. Also, fucoidan directly increased SR‐B1 expression and which was associated with p38 MAPK activation. Overall, p38 MAPK, AP‐1, and IRF‐1 play an important role in the inhibitory effect of fucoidan on T/I‐stimulated NO production, and intracellular SR‐B1 expression may be related to the inhibition of iNOS expression by fucoidan via regulation of p38‐p. Fucoidan could be a potential therapeutic agent for treating inflammatory‐related neuronal injury in neurological disorders.(This work was supported by grant No. RTI05‐01‐02 from the Regional Technology Innovation Program of the Ministry of Konwledge Economy(MKE))