| 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. |
