n4-(2-2-dimethyl-3-oxo-4h-pyrid(1-4)oxazin-6-yl)-5-fluoro-n2-(3-4-5-trimethoxyphenyl)-2-4-pyrimidinediamine has been researched along with Proteinuria* in 1 studies
1 other study(ies) available for n4-(2-2-dimethyl-3-oxo-4h-pyrid(1-4)oxazin-6-yl)-5-fluoro-n2-(3-4-5-trimethoxyphenyl)-2-4-pyrimidinediamine and Proteinuria
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Effects of a spleen tyrosine kinase inhibitor on progression of the lupus nephritis in mice.
The Fc receptors (FcR) have pivotal roles in the pathogenesis of the autoimmune glomerulonephritis. We therefore investigated the effects of a Syk inhibitor on the progression of lupus nephritis and SH3 domain binding protein 2 and p38MAP kinase signalings in mice. NZB/W F1 mice, a model of lupus nephritis, received a Syk inhibitor R406. Western blotting and immunohistochemistry revealed that R406 treatment significantly delayed the appearance of proteinuria, histologically improved their glomerulosclerosis and inhibited the increased the expression of MCP-1 and TGF-β1 mRNAs and the nephrin and podocin proteins in the kidney. The treatment suppressed the phosphorylation of 3BP2 in white blood cells from the spleen and significantly inhibited the phosphorylation of p38MAPK in the kidney but did not affect expression of neonatal Fc receptor. These findings indicate the important roles and mechanisms of Fcγ receptors I and III in the development of autoimmune glomerulonephritis and suggest the possible application of Syk inhibitors as novel medicines for the glomerulonephritis. Topics: Administration, Oral; Animals; Chemokine CCL2; Disease Progression; Enzyme Inhibitors; Female; Humans; Intracellular Signaling Peptides and Proteins; Kidney; Lupus Nephritis; Membrane Proteins; Mice; Mice, Inbred NZB; Oxazines; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Protein Kinase Inhibitors; Proteinuria; Pyridines; Receptors, IgG; Signal Transduction; Syk Kinase; Transforming Growth Factor beta1 | 2017 |