Hypoxia/reoxygenation stimulates endothelial cells to promote interleukin-1 and interleukin-6 production. Effects of free radical scavengers
| Autor: | J. Dornand, O. Palluy, Claude Bonne, J. Favero, Y. Ala, G. Modat |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Umbilical Veins
Endothelium Free Radicals medicine.medical_treatment Immunology Inflammation Toxicology Umbilical vein Oxygen Consumption medicine Humans Pharmacology (medical) Interleukin 6 Cells Cultured Pharmacology Glutathione Peroxidase biology Chemistry Interleukin-6 Superoxide Dismutase Interleukin Free Radical Scavengers Hypoxia (medical) Molecular biology Cell Hypoxia medicine.anatomical_structure Cytokine biology.protein Human umbilical vein endothelial cell Endothelium Vascular medicine.symptom Interleukin-1 |
| Zdroj: | Agents and actions. 37(1-2) |
| ISSN: | 0065-4299 |
| Popis: | Vascular endothelium produces and/or interferes with various cytokines. Previous studies have demonstrated interactions of these inflammatory and immunological mediators with oxygen-derived free radicals. The present work examines the relationship between hypoxia/reoxygenation (H/R) and cytokine production by cultured endothelial cells. Human umbilical vein endothelial cell (HUVEC) monolayers were incubated for 24 h in normoxia or submitted to 5 h hypoxia/19 h reoxygenation. Then, interleukin-1 (IL-1) alpha and beta, and interleukin-6 (IL-6), were measured in culture supernatants by specific enzyme immunoassays and bioassays, respectively. Under these conditions, the spontaneous production of IL-1 and IL-6, detected in normoxic HUVEC, greatly increased after H/R treatment. The observed enhancement was cycloheximide-sensitive and, consequently, reflected a de novo protein synthesis. Superoxide dismutase and glutathione peroxidase prevented H/R-induced IL-1 and IL-6 increase. These results constitute the first demonstration that H/R stimulates HUVEC to promote IL-1 and IL-6 production and strongly suggest a role for oxygen-derived free radicals in the cytokine synthesis. |
| Databáze: | OpenAIRE |
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