AI Article Synopsis
- - The study aims to explore how the NF-kappaB/IkappaB signaling pathway influences the production of monocyte chemoattractant protein-1 (MCP-1) in rat models of glomerulonephritis.
- - Researchers induced nephrotoxic serum nephritis (NTN) and used various assays to measure NF-kappaB activation, nuclear p65 movement, and degradation of specific proteins in renal tissue, finding significant changes compared to controls.
- - Results showed increased MCP-1 levels in kidney tissue, with notable activation of the NF-kappaB pathway, suggesting its critical role in the development of glomerulonephritis.
Article Abstract
Objective: To investigate the role of NF-kappaB/IkappaB signal pathway in mediating the expression of monocyte chemoattractant protein-1 (MCP-1) in experimental rat glomerulonephritis.
Methods: Nephrotoxic serum nephritis (NTN) was induced by injection of anti-GBM antibody into the tail veins of rats. Electrophoretic mobility shift assay (EMSA) and Western Blot were used to detect the activation of NF-kappaB, nuclear translocation of p65 subunit and degradation of IkappaBalpha and IkappaBbeta in rat renal tissue. MCP-1 expression in glomeruli and renal tubules was also assessed by immunohistochemistry and ribonuclease protection assay. This was further correlated with the activation of NF-kappaB.
Results: There was an obvious expression of MCP-1 in glomeruli and renal tubules. Significant up-regulation of NF-kappaB activation, nuclear translocation of p65 subunit, and degradation of IkappaBalpha and IkappaBbeta were also observed in NTN rat renal tissue, as compared to the control group. A positive correlation was noted between NF-kappaB activation and MCP-1 expression.
Conclusions: NF-kappaB/IkappaB signal pathway may play an important pathogenetic role in glomerulonephritis, with mediating the expression of MCP-1.
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