Abstract
Interaction between adipocytes and macrophages contributes to the development of insulin resistance in obese adipose tissues. In this study, we examined whether luteolin, food-derived flavonoid, could suppress the production of inflammatory mediators of the interaction between adipocytes and macrophages. Experiments using a coculture system of adipocytes and macrophages showed that luteolin suppressed the production of inflammatory mediators. In addition, activated macrophages were targets for the suppressive effect of luteolin. Luteolin inhibited the phosphorylation of JNK and suppressed the production of inflammatory mediators in the activated macrophages. The findings indicate that luteolin can inhibit the interaction between adipocytes and macrophages to suppress the production of inflammatory mediators, suggesting that luteolin is a valuable food-derived compound for the treatment of metabolic syndrome.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3T3-L1 Cells
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Adipocytes / cytology
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Adipocytes / drug effects*
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Adipocytes / metabolism
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Animals
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Blotting, Western
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Cell Communication / drug effects
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Cell Line
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Coculture Techniques
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Culture Media, Conditioned / pharmacology
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Dose-Response Relationship, Drug
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Enzyme Activation / drug effects
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Enzyme-Linked Immunosorbent Assay
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Flavonoids / pharmacology
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Food
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I-kappa B Proteins / metabolism
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Inflammation Mediators / metabolism
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JNK Mitogen-Activated Protein Kinases / metabolism*
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Luteolin / pharmacology*
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Macrophages / cytology
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Macrophages / drug effects*
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Macrophages / metabolism
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Mice
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Reverse Transcriptase Polymerase Chain Reaction
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Tumor Necrosis Factor-alpha / genetics
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Culture Media, Conditioned
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Flavonoids
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I-kappa B Proteins
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Inflammation Mediators
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Tumor Necrosis Factor-alpha
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JNK Mitogen-Activated Protein Kinases
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Luteolin