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Lipid extracts from edible blue‐green algae reduce the production of pro‐inflammatory cytokines by inhibiting nuclear translocation of NF‐κB in RAW 264.7 macrophages
Author(s) -
Ku Chai Siah,
Lee Jiyoung
Publication year - 2012
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.26.1_supplement.823.44
Subject(s) - proinflammatory cytokine , tumor necrosis factor alpha , inflammation , cytokine , lipopolysaccharide , interleukin 6 , biology , chromosomal translocation , interleukin , chemistry , pharmacology , biochemistry , immunology , gene
Chronic inflammation contributes to the pathogenesis of several metabolic diseases including atherosclerosis. We investigated anti‐inflammatory effects of lipid extract from edible blue‐green algae (BGA) such as Nostoc commune var. Sphaeroides Kützing (NO) and Spirulina Platensis (SP) in RAW 264.7 macrophages. The algal lipids were extracted into chloroform/methanol (2:1). Cells were pre‐treated with 100 μg/ml of the lipid extract for 12 hr and subsequently activated by 100 ng/ml lipopolysaccharide for 18 hr. Quantitative realtime PCR analysis showed that mRNA levels of pro‐inflammatory cytokines such as tumor necrosis factor α, interleukin 1β, and interleukin 6 are significantly repressed by NO and SP lipid extract. Cytokine array demonstrated that the secretion of pro‐inflammatory cytokines was also markedly reduced by both NO and SP lipid extract. The repressive effect was at least partly due to the inhibition of nuclear translocation of NF‐ κB. In addition, the repression of pro‐inflammatory cytokine expression by algal extracts was more potent than SN50, an inhibitor of NF‐κB nuclear translocation, suggesting that additional pathways may exist for the anti‐inflammatory effect of NO and SP lipid extract. In conclusion, BGA lipid extract contains anti‐inflammatory compounds that could be developed as a nutraceutical agent against inflammation‐related diseases. Grant Funding Source : NIH R21AT005152