Abstract
Microglia, brain inflammatory cells, are activated in injured brain and function similar to macrophages. The activated microglia produce nitric oxide (NO), a major toxic substance from these cells, by inducing expression of inducible NO synthase (iNOS). In this study, we found that sphingomyelinase (SMase) alone induced NO release/iNOS mRNA expression in cultured rat brain microglia. On the contrary to SMase, however, membrane-permeable c2-ceramide had little effect on NO release/iNOS mRNA expression. Fumonisin B1, an inhibitor of de novo synthesis of ceramide, did not reduce lipopolysaccharide (LPS)-induced NO release. However, neither SMase nor c2-ceramide enhanced LPS- or Abeta (25-35)-induced NO release/iNOS mRNA expression.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid beta-Peptides / pharmacology
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Animals
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Carboxylic Acids / pharmacology
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Cells, Cultured
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Enzyme Inhibitors / pharmacology
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Fumonisins*
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Gene Expression Regulation, Enzymologic / drug effects
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Lipopolysaccharides / pharmacology
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Microglia / cytology
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Microglia / enzymology*
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Nitric Oxide Synthase / genetics*
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Nitric Oxide Synthase Type II
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Peptide Fragments / pharmacology
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RNA, Messenger / analysis
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Rats
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Rats, Sprague-Dawley
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Sphingomyelin Phosphodiesterase / pharmacology*
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Sphingosine / analogs & derivatives*
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Sphingosine / pharmacology*
Substances
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Amyloid beta-Peptides
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Carboxylic Acids
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Enzyme Inhibitors
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Fumonisins
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Lipopolysaccharides
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N-acetylsphingosine
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Peptide Fragments
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RNA, Messenger
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amyloid beta-protein (25-35)
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fumonisin B1
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type II
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Nos2 protein, rat
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Sphingomyelin Phosphodiesterase
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Sphingosine