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.
journal_name
Immunologyjournal_title
Immunologyauthors
Bricio T,Molina A,Martin A,Mampaso Fsubject
Has Abstractpub_date
1994-01-01 00:00:00pages
53-7issue
1eissn
0019-2805issn
1365-2567journal_volume
81pub_type
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