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Expression of pro‐inflammatory mediators was reduced by lipid extract of Nostoc commune, a blue‐green alga, through the inhibition of nuclear factor kappa B (NF‐kB) pathway in RAW 264.7 macrophages
Author(s) -
Park YoungKi,
Rasmussen Heather E.,
Ehlers Sarah J.,
Lu Fan,
Schlegel Vicki L.,
Carr Timothy P.,
Lee JiYoung
Publication year - 2007
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.21.5.a365-a
Subject(s) - fatty acid , tumor necrosis factor alpha , biochemistry , lipopolysaccharide , chemistry , interleukin 8 , microbiology and biotechnology , biology , inflammation , immunology
We investigated anti‐inflammatory effect of Nostoc commune lipid extract (NLE) in RAW 264.7 macrophages. Cells were incubated with NLE (0‐100 μg/ml) and activated by lipopolysaccharide. Realtime PCR was performed to measure mRNA abundance of pro‐inflammatory mediators, including tumor necrosis factor α (TNFα), cyclooxygenase 2 (COX2), interleukin‐1β (IL‐1β), IL‐6 and inducible nitric oxide synthase. Expression of the pro‐inflammatory mediators was drastically reduced by the addition of NLE in a dose‐dependent manner. Secretion of TNFα and IL‐1β in the medium was decreased by NLE based on ELISA assay. Thin‐layer chromatography and gas chromatography analyses of NLE revealed that it contains 15% fatty acids, 75% of which are unsaturated fatty acids. To determine whether the inhibition of pro‐inflammatory mediator production by NLE is primarily attributed to its fatty acid content, we incubated macrophages with 15% of fatty acid mixture, which was formulated to reflect fatty acid composition of NLE. Fatty acid mixture reduced mRNA of TNFα and COX2, but to a lesser extent than did NLE, suggesting the presence of bioactive compounds with an anti‐inflammatory property in NLE. NF‐κB p65 DNA binding activity was significantly reduced by the addition of NLE. The data suggest that NLE contains bioactive compounds with anti‐inflammatory function, at lease in part, by the inhibition of NF‐κB pathway. (Supported by NSF‐EPSCoR grant EPS‐0346476)