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Sphingomyelinase but not ceramide induces nitric oxide synthase expression in rat brain microglia.

Authors
Yang, MS; Jou, I; Inn-Oc, H; Joe, E
Citation
Neuroscience letters, 311(2):133-136, 2001
Journal Title
Neuroscience letters
ISSN
0304-39401872-7972
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.
MeSH terms
Amyloid beta-Peptides/pharmacologyAnimalsCarboxylic Acids/pharmacologyCells, CulturedEnzyme Inhibitors/pharmacologyFumonisins*Gene Expression Regulation, Enzymologic/drug effectsLipopolysaccharides/pharmacologyMicroglia/cytologyMicroglia/enzymology*Nitric Oxide Synthase/genetics*Nitric Oxide Synthase Type IIPeptide Fragments/pharmacologyRNA, Messenger/analysisRatsRats, Sprague-DawleySphingomyelin Phosphodiesterase/pharmacology*Sphingosine/analogs & derivatives*Sphingosine/pharmacology*
PMID
11567796
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
주, 일로조, 은혜
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