Abstract
In the present study, we demonstrate that sodium butyrate repressed IFN-gamma-induced expression of iNOS and TNF-alpha, but had little effect on LPS-induced expression in BV2 murine microglial cells. Sodium butyrate significantly inhibited NF-kappa B binding and NF-kappa B-mediated transcription induced by IFN-gamma, suggesting that the anti-inflammatory effect of sodium butyrate is mediated via specific inhibition of the NF-kappa B pathway. IFN-gamma is a major stimulator of innate and adaptive immune response. Thus, the specific down-regulation of IFN-gamma-induced microglial activation by sodium butyrate may provide potential therapeutic strategies for a variety of inflammatory diseases in the central nervous system.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blotting, Western
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Butyric Acid / pharmacology*
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Cells, Cultured
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Electrophoretic Mobility Shift Assay
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Enzyme-Linked Immunosorbent Assay
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Interferon-gamma / drug effects*
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Interferon-gamma / metabolism
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Lipopolysaccharides / pharmacology*
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Mice
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Microglia / drug effects*
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Microglia / metabolism
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NF-kappa B / drug effects
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NF-kappa B / metabolism
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Nitric Oxide / metabolism*
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Nitric Oxide Synthase / biosynthesis
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Nitric Oxide Synthase / drug effects
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Nitric Oxide Synthase Type II
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Recombinant Proteins
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Reverse Transcriptase Polymerase Chain Reaction
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Signal Transduction / immunology
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Transfection
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Tumor Necrosis Factor-alpha / drug effects
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Tumor Necrosis Factor-alpha / metabolism*
Substances
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Lipopolysaccharides
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NF-kappa B
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Recombinant Proteins
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Tumor Necrosis Factor-alpha
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Butyric Acid
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Nitric Oxide
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Interferon-gamma
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type II
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Nos2 protein, mouse