Nephroprotective effects of diminazene on doxorubicin-induced acute kidney injury in rats

Figures

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  Fig. 1. The effect of diminazene (DM, 15 mg/kg), lisinopril (LS, 10 mg/kg), and valsartan (VL, 30 mg/kg) on the following parameters in rats subjected to doxorubicin (DOX, 13.5 mg/kg) treatment: A. The urinary albumin/creatinine ratio B. Creatinine clearance C. Urinary N-Acetyl-β-D-Glucosaminidase (NAG)/creatinine ratio. DM, LS, and VL were administered orally to the rats throughout the experiment's duration. Acute Kidney Injury (AKI) was induced through a single intraperitoneal injection of DOX on the 6th day of the study. Urine samples were collected from the rats on the 9th day while they were placed in metabolic cages. The data provided represents the means with standard error of the mean (SEM) and is based on a sample size of six (n = 6).

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  Fig. 2. The effect of diminazene (DM, 15 mg/kg), lisinopril (LS, 10 mg/kg) and valsartan (VL, 30 mg/kg) on the levels of the following parameters in rats exposed to doxorubicin (DOX) treatment: A. Blood uric acid; B. Interleukin-1β (IL-1β); C. Tumor necrosis factor-alpha (TNF-α). Throughout the duration of the experiment, DM, LS, and VL were orally administered to the rats. Acute Kidney Injury (AKI) was induced by a single intraperitoneal injection of DOX at a dose of 13.5 mg/kg on the 6th day of the study. The data provided represents the means along with their standard error of the mean (SEM) based on a sample size of six (n = 6).

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  Fig. 3. The effect of diminazene (DM, 15 mg/kg), lisinopril (LS, 10 mg/kg) and valsartan (VL, 30 mg/kg) on A. Renal superoxide dismutase (SOD); B. Glutathione reductase (GR); C. Catalase; and D. Malondialdhyde (MDA) in rats treated with doxorubicin (DOX). Throughout the experiment, DM, LS, and VL were given orally to rats. AKI was caused by a single intraperitoneal injection of DOX (13.5 mg/kg) on the 6th day of the experiment. The data provided represents the means along with their standard error of the mean (SEM) based on a sample size of six (n = 6).

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  Fig. 4. Microscopic images of the renal cortex (Scale Bar= 100 µm, A-E: H&E, F-J: Picro-Sirius red staining). (A) Control group displaying regular renal histology characterized by intact glomerular tufts and renal tubules (lesion score 0). (B) Doxorubicin (DOX) group showcasing pronounced cystic dilatation (marked by asterisk), basophilia, necrosis (indicated by arrow) of renal tubules, and the presence of tubular casts (arrowheads) along with shrunken glomeruli (lesion score 4). (C) DOX plus diminazene group presenting significant basophilia of renal tubules (arrow) along with the presence of tubular casts (arrowhead) and intact glomerular tufts (lesion score 2). (D) DOX plus lisinopril group demonstrating dilatation (asterisk) and necrosis (arrow) of a few renal tubules while maintaining intact glomeruli (lesion score 3). (E) DOX plus valsartan group displaying basophilia of renal tubules (arrows) with intact glomeruli (lesion score 2). (F-J) Depicting the distribution of collagen fibers stained in red and non-collagen structures stained in yellow in all five groups.