الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Kidney diseases pose a worldwide health problem and have led to significant morbidity and mortality among kidney disease patients. The current study aimed to explore the potential renoprotective impact of lactoferrin (LF) in two different rat models of acute and chronic kidney diseases compared to the standard renoprotective selenium nanoparticles (SeNPs). Both AKI and CKD manifestations were confirmed by the significant increase in renal somatic index, serum creatinine, blood urea nitrogen, proteinuria, and albuminuria with the concomitant significant reduction in creatinine clearance. Moreover, incidence of oxidative injury was confirmed by the marked elevation in renal MDA content and TXNIP concentration with the profound decline in renal GSH concentration, retracted SOD activity, TAC, and renal NRF2 expression. Serum levels of IL-1β, renal expression of TXNIP, NLRP3, CD68 and NF-κB significantly escalated as well. Furthermore, the onset of fibrosis in CKD model was confirmed by the marked increase in renal TGF-β1 expression and the increased renal hydroxyproline contents along with Masson’s trichrome stained-extracellular matrix components in renal sections. Finally, the apoptotic signaling was confirmed by the marked increase in renal caspase-3 expression in both models. In conclusion, LF revealed a significant dose-dependent renoprotective impact against both GLY- and AD-induced AKI and CKD. Noteworthy, LF (300 mg/kg) was the only dose with renoprotective impact comparable to the standard reference renoprotective SeNPs. The renoprotective impact is primarily mediated by its anti-inflammatory, antioxidant, anti-apoptotic, and anti-fibrotic properties. Thus, LF can be proposed as an add-on therapy and an attractive approach to attenuate both AKI and CKD especially in high-risk individuals. Further clinical studies are required to specify the exact effective therapeutic doses to human beings.