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 Aβ (25–35)-induced NO release/iNOS mRNA expression.
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