Study on the Regulation of Compound siRNA Nanoparticles on the Rat Model of Kidney Injury Induced by Sepsis by Inhibiting the Expression of NF-κB and P65.

Abstract

This article explores the pathogenesis of sepsis AKI, and seeks to protect the acute damage of sepsis tissues and organs. This study is to prepare a rat sepsis-induced AKI model by CLP, and to observe the pathological changes of kidney tissue and the function of kidney changes, and observe the effect of siRNA nanoparticles on its intervention, preliminary explore the protective effect and possible mechanism of siRNA nanoparticles on AKI in sepsis rats, and provide more information for the clinical treatment of siRNA nanoparticles in sepsis theoretical and experimental basis. We analysis the benefit and deficiency of nuclear factor-κB (NF-κB) activation in the pathogenesis of glomerulonephritis and its regulatory effect on NF-κB activation. In the rat model group, no treatment was given after injection of nephrotoxic serum, and the rats were sacrificed on the 14th day; the compound siRNA nanoparticle intervention group (treatment group) was given dexamethasone 0.125 daily on the 1st to 14th day after nephrotoxic serum injection. Immunohistochemistry and medical image analysis system were used to observe NF-κB activation of monocyte chemotactic protein-1 (MCP-1) in glomeruli and tubules, and analyze their relationship with proteinuria and glomerular cells. The results showed that the expression of NF-κB in the glomeruli and tubules of the model group was significantly up-regulated regarding to the control group, and MCP-1's expression in the glomeruli and tubules of the model group was higher than that of the control group. The activation of NF-κB and the expression of MCP-1 in glomeruli are closely related to monocyte infiltration and proteinuria; NF-κB activation and MCP-1 expression in glomeruli and tubules of the compound siRNA nanoparticles intervention group were significantly down-regulated. It was concluded that the activation of NF-κB has great impact on the pathogenesis of glomerulonephritis, and inhibition of NF-κB activation may be one of the mechanisms of anti-nephritis effect.