الفهرس 
AcknowledgementOnly 14 pages are availabe for public view
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Abstract
This current study aimed to discuss the possible modulatory effects of dasatinib (DAS) and nifuroxazide (NIF) in reversing and modifying the nephron ҆s functions and architecture in a chronic kidney disease (CKD) model progressed to renal interstitial fibrosis (RIF)-induced by ureteral obstruction to the left ureter in males Sprague-Dawley (SD) rats. The other half was preserved in phosphate buffer solution (PBS) PH 7.4 at -80°C ,then the kidney homogenate was prepared for determination of renal oxidative/antioxidative stress biomarkers; MDA, GSH concentration and SOD activity. Enzyme linked immunosorbent assay (ELISA) was used for assessment of renal protein expression of the pro-inflammatory cytokines; interleukin 1-β (IL-1β), tumor necrosis factor- α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and transforming growth factor–β1 (TGF-β1). Western blott (WB) was used for quantification of protein expression of renal inflammatory fibrotic parameters; phosphorylated/ total signal tranceducer and activator of transcription-3 (p-STAT-3/t-STAT-3 ratio), p-Src, Abelson tyrosine kinase (c-Abl), and nuclear factor- κB P65 (NF-κB P65). Unilateral ureteral obstruction to the left ureter has been reported to be a classical model for induction of RIF in an accelerated manner. The present study showed marked renal injury indicated by increased left kidney mass index in comparison to the right one. Urine output, creatinine clearance and serum albumin decreased. On the other hand, total protein and urinary albumin excretion, serum creatinine, serum uric acid and BU were elevated. In conclusion the current study sheds light on the potential roles of DAS and NIF as renoprotective agent and its roles in reversing renal fibrosis induced as an end stage to CKD. NIF supposed the better agent due to its effectiveness in attenuation of RIF through modulation of STAT-3/NFϰBP65 pathway, its safety profile and low cost when compared to DAS.