Effect of suramin on renal proximal tubular cells damage induced by cisplatin in rats (histological and immunohistochemical study)

Abstract

Background:Renal toxicity is the most common complication of cispaltin therapy that has broad-spectrum antitumor activity against a variety of human solid tumor. Suramin, a Food and Drug Administration-approved old drug is a polysulfonated compound of napthylurea originally designed to treat trypanosomiasis.Aim:The current work aimed to investigate the possible protective effect of different doses of suramin against cisplatin-induced renal proximal tubular cells (RPTCs) damage.Material and Methods:Fifty adult male rats were used and divided into five equal groups. Group I served as a control, group II received suramin alone (10 mg/kg). Groups III, IV and V were administered cisplatin once (5 mg/kg, intraperitoneally) alone or combined with low dosage suramin (5 mg/kg) or high dosage suramin (10 mg/kg) once intravenously respectively.Results:Compared with control rats, cisplatin administration caused proximal tubules damage, RPTCs vacuolation with pyknotic nuclei, loss of brush border and widespread caspase-3 immunostaining. Cisplatin-induced RPTCs toxicity was further confirmed morphometrically (a significantly decreased proximal tubular epithelium height and increased mean number of caspase-3-immunopositive cells). These changes were accompanied by biochemical alteration manifested as a significant increase of blood urea nitrogen and serum creatinine. Simultaneous administration of high-dose but not low-dose suramin to the cisplatin-treated rats improved the deleterious morphological and morphometrical effects on RPTCs and restored the aforementioned biochemical parameters to control values.Conclusion:In conclusion suramin in a dose dependant manner protects RPTCs from damage induced by cisplatin.

Protective Potential of Lycopene Enriched Tomato Extract against Dexamethasone Induced Hepatic and Renal Damage in Mice

“…Light microscopy studies of hepatic and renal tissues indicated marked damage in these tissues in DEX group. Such deviations in histoarchitecture signifying damage have been reported previously [29,[88][89][90]. The tissue sections from LycT+DEX group revealed less damage as compared to the DEX group.…”

Anti‐Inflammatory and Antioxidative Properties of Isoflavones Provide Renal Protective Effects Distinct from Those of Dietary Soy Proteins against Diabetic Nephropathy

“…In STZ‐induced diabetic rat models, isoflavones intake for 8 weeks increased the serum insulin level and reduced serum glucose, [ 21 ] genistein treatment showed protective and regenerative effects in pancreatic β‐cells. [ 22 ] Isoflavones supplementation failed to inhibit hyperglycaemia in KKAy mice, unlike in type 1 diabetes model, probably due to a pancreatic injury in this T2D model. Additionally, genistein reduced renal tubular cell death caused by ischemia/reperfusion injury [ 23 ] and cisplatin‐induced injury.…”

Amphora algae with low‐level ionizing radiation exposure ameliorate D‐galactosamine‐induced inflammatory impairment in rat kidney

“…d ‐GalN induced liver injury and the development of renal failure in experimental animals as indicated by Gezginci‐Oktayoglu et al, 38 Hao et al 39 and El‐Kordy 11,40 . Also, it was shown that acute liver failure is accompanied by renal failure in 50% to 80% of patients 41,42 and declined renal blood flow that indicates renal vasoconstriction 43 .…”

“…D-GalN induced liver injury and the development of renal failure in experimental animals as indicated by Gezginci-Oktayoglu et al, 38 Hao et al 39 and El-Kordy. 11,40 Also, it was shown that acute liver failure is accompanied by renal failure in 50% to 80% of patients 41,42 and declined renal blood flow that indicates renal vasoconstriction. 43 Anand et al 15 Treatment with D-GalN resulted also in a significant increase of serum urea, creatinine, cystatin-C and neutrophil gelatinase-associated lipocalin levels which agrees with Ayhanci et al, 16 Sinha et al, 46 Dokumacioglu et al 47 Inflammation is a key factor in the pathogenesis of renal disease and it's progression.…”