Effects Of Alterations Of Glomerular Fibrin Deposition On Renal Inflammation In Rats At Different Age Stages

Background. Intraglomerular fibrin deposition has been observed in most types of human glomerulonephritis and associated with glomerular injury. Recent data indicated that aging accelerated glomerular fibrin deposition induced by lipopolysaccharide (LPS) in mice, and that fibrin could directly activate endothelial cell in vitro. However, the mechanisms for aging acceleration glomerular fibrin deposition and the effects of aging on inflammation induced by glomerular fibrin deposition remain unclear. So in the present study, our hypothesis was that aging can contribute to glomerular fibrin deposition by upregulating renal tissue plasminogen activator inhibitor and or downregulating anticoagulatant, and that aging may exacerbate glomerular inflammatory responses induced by glomerular fibrin deposition. Objective. To test our hypothesis, glomerular fibrin deposition was induced by LPS administration and to explore the mechanism for aging contributing glomerular fibrin deposition. Furthermore, glomerular fibrin deposition was controlled by pharmaceutical methods, to determine the effects of aging on renal inflammation induced by glomerular fibrin deposition. Methods. Glomerular fibrin deposition were detected by immunofluorescence staining and analyzed by laser scanning confocal microscopy. The expressions of protein and gene were determined by immunochemohistory staining, Western blot and Northern blot. Both young and aged rats with glomerular fibrin deposition induced by LPS were treated with tranexamic acid (TA) and TA plus urokinase (UK). Comparisons were made between three treatment groups within the same age groups, as well as between two age groups with a same treatment. Results. Glomerular fibrin deposition of aged LPS group was significantly higher than that of young LPS group, while renal PAI-1 protein and gene expression of aged LPS group were higher than that...