Abstract
Doxorubicin-stimulated whole rat glomeruli and dissociated mesangial and resident glomerular macrophage cells produced the release of interleukin (IL)-1 beta cytokine. This activity increased after the addition of lipopolysaccharide (LPS) or LPS plus indomethacin to the cultures. In the presence of WEB2086 [platelet-activating factor (PAF)-acether antagonist], this activity showed a drastic reduction, without modification after sodium furegrelate (thromboxane synthetase inhibitor) was added to the cultures. Our results also demonstrate that this IL-1 beta activity is mainly produced by glomerular-resident macrophage cells. These findings support the important role by both IL-1 beta and PAF-acether mediator factors, at the cellular level, in the rat model of doxorubicin-induced nephrosis.
MeSH Terms
Animals
Azepines/pharmacology
Cells, Cultured
Dose-Response Relationship, Drug
Doxorubicin/pharmacology
Drug Interactions
Glomerular Mesangium/drug effects,immunology
Interleukin-1/chemistry,metabolism
Kidney Glomerulus/drug effects,immunology
Kinetics
Lipopolysaccharides/pharmacology
Male
Molecular Weight
Platelet Activating Factor/antagonists & inhibitors
Rats
Rats, Sprague-Dawley
Triazoles/pharmacology
Chemicals
Azepines
Interleukin-1
Lipopolysaccharides
Platelet Activating Factor
Triazoles
WEB 2086
Doxorubicin
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Bricio T
Department of Pathology, Hospital Ramon y Cajal, Madrid, Spain.
Molina A
Martin A
Mampaso F
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