Erythropoietin decreases cytotoxicity and nitric oxide formation induced by inflammatory stimuli in rat oligodendrocytes
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
15857166
DOI
10.33549/physiolres.930749
PII: 749
Knihovny.cz E-resources
- MeSH
- Erythropoietin pharmacology MeSH
- Interferon-gamma MeSH
- Rats MeSH
- Cells, Cultured MeSH
- Lipopolysaccharides MeSH
- RNA, Messenger metabolism MeSH
- Brain MeSH
- Neuroprotective Agents pharmacology MeSH
- Animals, Newborn MeSH
- Oligodendroglia drug effects metabolism MeSH
- Nitric Oxide biosynthesis metabolism MeSH
- Rats, Wistar MeSH
- Gene Expression Regulation MeSH
- Nitric Oxide Synthase Type II biosynthesis metabolism MeSH
- Cell Survival MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Erythropoietin MeSH
- Interferon-gamma MeSH
- lipopolysaccharide, E. coli O26-B6 MeSH Browser
- Lipopolysaccharides MeSH
- RNA, Messenger MeSH
- Neuroprotective Agents MeSH
- Nos2 protein, rat MeSH Browser
- Nitric Oxide MeSH
- Nitric Oxide Synthase Type II MeSH
In the present study, we investigated whether erythropoietin (Epo) has a protective effect against cytotoxicity induced by interferon-gamma (IFN-gamma ) and lipopolysaccharide (LPS) in primary rat oligodendrocyte cultures. The possible modulatory effect of erythropoietin on inducible nitric oxide synthase (iNOS) mRNA expression and nitrite production were also analyzed. Erythropoietin exerted a significant protective effect against IFN-gamma and LPS-induced oligodendrocyte injury as determined by lactate dehydrogenase assay. Treatment with erythropoietin inhibited the expression of iNOS mRNA and nitrite production resulting from proinflammatory stimulation by IFN-gamma and LPS. These results suggest that erythropoietin has protective effects against inflammatory oligodendrocyte injury in vitro and may play a protective role in neurological disorders characterized by oligodendrocyte death, such as multiple sclerosis.
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