Abstract

Introduction:Aminoglycoside-induced acute kidney injury (AKI) is a pathology closely linked to oxidative and inflammatory reactions. Taking into account the previous reported antioxidant and anti-inflammatory effects of D-005, a lipid extract obtained from Cuban palm Acrocomia crispa (Arecaceae) fruits, this work aimed to evaluate the effects of D-005 on kanamycin-induced AKI.Methods: Male Wistar rats were divided into 7 groups: negative control (vehicle, Tween 65/H2O) and six groups treated with kanamycin to induce AKI: positive control (vehicle), D-005 (25, 100, 200, and 400 mg/kg) and grape seed extract (GSE, 200 mg/kg). D-005, vehicle, and GSE oral treatments were administered once daily for seven days, 1 h before kanamycin (500 mg/kg, i.p.). Serum uric acid and urea concentrations, renal histopathology, and oxidative markers (malondialdehyde (MDA), sulfhydryl (SH) groups, and catalase (CAT) activity) were assessed.Results:D-005 significantly reduced uric acid and urea levels, starting from D-005 100 mg/kg. Histopathologically, D-005, at all the tested doses, protected renal parenchyma structures (glomeruli, proximal tubules, and interstitium). These findings were accompanied by a significant reduction of MDA and SH group concentrations as well as restoration of CAT activity. The highest percentages of inhibition were obtained with the dose of 400 mg/kg. GSE, the reference substance, also prevented kanamycin-induced biochemical and histopathological changes, as well as reduced MDA and SH groups and restored CAT activity.Conclusion:The administration of repeated oral doses of D-005 significantly protected against kanamycin-induced AKI, which could be associated with the antioxidant and anti-inflammatory effects of this extract.

Highlights

  • Aminoglycoside-induced acute kidney injury (AKI) is a pathology closely linked to oxidative and inflammatory reactions

  • The results of this study demonstrate the protective effect of repeated oral doses of D-005 on kanamycininduced AKI

  • The biochemical and histopathological changes in the positive control group is in accordance to those described by other authors under similar conditions[27,28]

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Summary

Introduction

Aminoglycoside-induced acute kidney injury (AKI) is a pathology closely linked to oxidative and inflammatory reactions. D-005, at all the tested doses, protected renal parenchyma structures (glomeruli, proximal tubules, and interstitium) These findings were accompanied by a significant reduction of MDA and SH group concentrations as well as restoration of CAT activity. Conclusion: The administration of repeated oral doses of D-005 significantly protected against kanamycin-induced AKI, which could be associated with the antioxidant and anti-inflammatory effects of this extract. Acute kidney injury (AKI) is a clinical syndrome of varied etiology characterized by a sudden decrease in kidney function, accumulation of waste metabolites, water-mineral imbalance, and systemic symptoms. It is a common problem in intensive care medicine since a moderate AKI increases the risk of death by approximately five times[1,2]. Tubular toxicity by AMG is mainly characterized by several pathological changes in tubular epithelial cells in the proximal segment, associated with an important inflammatory component followed by non-lethal functional alterations of key components involved in the transport of water and solutes[4,5]

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