Inhibition of the production of mediators of inflammation by corticosteroids is a glucocorticoid receptor-mediated process
| Autor: | G.S. Madretsma, C.J.A.M. Tak, Freek J. Zijlstra, Joanne Wilson, A. P. M. van Dijk |
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| Rok vydání: | 1996 |
| Předmět: |
endocrine system
medicine.medical_specialty medicine.medical_treatment Immunology Inflammation Peripheral blood mononuclear cell Steroid Glucocorticoid receptor Internal medicine lcsh:Pathology polycyclic compounds medicine Receptor Dexamethasone business.industry Ligand binding assay Antagonist Cell Biology Endocrinology lipids (amino acids peptides and proteins) medicine.symptom business hormones hormone substitutes and hormone antagonists Research Article lcsh:RB1-214 medicine.drug |
| Zdroj: | Mediators of Inflammation, Vol 5, Iss 2, Pp 100-103 (1996) Mediators of Inflammation |
| ISSN: | 1466-1861 0962-9351 |
| Popis: | In order to find an explanation for corticosteroid resistance we assessed whether inhibition by dexamethasone (DEX) of the stimulated production of TNF-∝, IL-6, PGE2and LTB4by peripheral blood mononuclear cells (MNC) depends on binding to the glucocorticoid receptor (GR), and whether it is determined by the number or the affinity of the GR of these cells. GR number and affinity of MNC were determined by means of a whole cell DEX binding assay. MNC were incubated with DEX and LPS or A23187 in the absence or presence of RU486, a potent steroid antagonist. DEX caused a concentration dependent inhibition of TNF-∝, IL-6 and PGE2production but had no effect on LTB4production. RU486 significantly blocked the effect of DEX, but no correlations were found between the inhibition of mediator release and the Kdor receptor number. |
| Databáze: | OpenAIRE |
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