Yang M S, Jou I, Inn-Oc H, Joe E
Department of Neuroscience, Ajou University School of Medicine, 442-721, Suwon, South Korea.
Neurosci Lett. 2001 Sep 28;311(2):133-6. doi: 10.1016/s0304-3940(01)02162-0.
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.
