Erythropoietin decreases cytotoxicity and nitric oxide formation induced by inflammatory stimuli in rat oligodendrocytes
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
15857166
DOI
10.33549/physiolres.930749
PII: 749
Knihovny.cz E-zdroje
- MeSH
- erythropoetin farmakologie MeSH
- interferon gama MeSH
- krysa rodu Rattus MeSH
- kultivované buňky MeSH
- lipopolysacharidy MeSH
- messenger RNA metabolismus MeSH
- mozek MeSH
- neuroprotektivní látky farmakologie MeSH
- novorozená zvířata MeSH
- oligodendroglie účinky léků metabolismus MeSH
- oxid dusnatý biosyntéza metabolismus MeSH
- potkani Wistar MeSH
- regulace genové exprese MeSH
- synthasa oxidu dusnatého, typ II biosyntéza metabolismus MeSH
- viabilita buněk MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- erythropoetin MeSH
- interferon gama MeSH
- lipopolysaccharide, E. coli O26-B6 MeSH Prohlížeč
- lipopolysacharidy MeSH
- messenger RNA MeSH
- neuroprotektivní látky MeSH
- Nos2 protein, rat MeSH Prohlížeč
- oxid dusnatý MeSH
- synthasa oxidu dusnatého, typ 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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