TY - JOUR
T1 - Protective effect of apocynin, a NADPH-oxidase inhibitor, against contrast-induced nephropathy in the diabetic rats
T2 - A comparison with n-acetylcysteine
AU - Ahmad, Akbar
AU - Mondello, Stefania
AU - Di Paola, Rosanna
AU - Mazzon, Emanuela
AU - Esposito, Emanuela
AU - Catania, Maria Antonietta
AU - Italiano, Domenico
AU - Mondello, Patrizia
AU - Aloisi, Carmela
AU - Cuzzocrea, Salvatore
N1 - Funding Information:
This study was supported by a grant from IRCCS Centro Neurolesi “Bonino-Pulejo” .
Copyright:
Copyright 2012 Elsevier B.V., All rights reserved.
PY - 2012/1/14
Y1 - 2012/1/14
N2 - The aim of this study was to investigate the effects of apocynin, a NADPH (nicotinamide adenine dinucleotide phosphate)-oxidase inhibitor, in diabetic rats with nephropathy induced by contrast medium (CIN). Diabetes was induced in male Wistar rats by a single dose of streptozotocin (60 mg/kg i.v.). Animals were then divided into the following groups: 1) control group (diabetic rats treated i.v. with saline solution); 2) iomeprol group (iomeprol at 10 ml/kg was injected i.v. 30 min after saline administration); 3) apocynin group (identical to the iomeprol group, except for pre-treatment with apocynin 5 mg/kg i.v., 30 min before iomeprol injection) and 4) N-acetylcysteine group (NAC) (same as iomeprol group, except for the treatment with NAC 20 mg/kg i.v. 30 min before iomeprol injection). CIN in animals were assessed 24 h after administration of iomeprol. Apocynin significantly attenuates the impaired glomerular function, concentration of Na +, K +, alpha glutathione S-transferase levels in urine and neutrophil gelatinase-associated lipocalin levels in plasma caused by iomeprol. In kidney, immunohistochemical analysis of some inflammatory mediators, such as nitrotyrosine, poly-ADP-ribosyl polymerase, tumor necrosis factor-α, interleukin-1β as well as apoptosis (evaluated as terminal deoxynucleotidyltransferase-mediated UTP end labeling assay) revealed positive staining in tissue obtained from iomeprol group. These parameters were markedly reduced in animals treated with apocynin. Similarly, these parameters were also markedly modified by NAC pre-treatment. Here, we have shown that apocynin attenuates the degree of iomeprol-induced nephropathy in diabetic rats.
AB - The aim of this study was to investigate the effects of apocynin, a NADPH (nicotinamide adenine dinucleotide phosphate)-oxidase inhibitor, in diabetic rats with nephropathy induced by contrast medium (CIN). Diabetes was induced in male Wistar rats by a single dose of streptozotocin (60 mg/kg i.v.). Animals were then divided into the following groups: 1) control group (diabetic rats treated i.v. with saline solution); 2) iomeprol group (iomeprol at 10 ml/kg was injected i.v. 30 min after saline administration); 3) apocynin group (identical to the iomeprol group, except for pre-treatment with apocynin 5 mg/kg i.v., 30 min before iomeprol injection) and 4) N-acetylcysteine group (NAC) (same as iomeprol group, except for the treatment with NAC 20 mg/kg i.v. 30 min before iomeprol injection). CIN in animals were assessed 24 h after administration of iomeprol. Apocynin significantly attenuates the impaired glomerular function, concentration of Na +, K +, alpha glutathione S-transferase levels in urine and neutrophil gelatinase-associated lipocalin levels in plasma caused by iomeprol. In kidney, immunohistochemical analysis of some inflammatory mediators, such as nitrotyrosine, poly-ADP-ribosyl polymerase, tumor necrosis factor-α, interleukin-1β as well as apoptosis (evaluated as terminal deoxynucleotidyltransferase-mediated UTP end labeling assay) revealed positive staining in tissue obtained from iomeprol group. These parameters were markedly reduced in animals treated with apocynin. Similarly, these parameters were also markedly modified by NAC pre-treatment. Here, we have shown that apocynin attenuates the degree of iomeprol-induced nephropathy in diabetic rats.
KW - Apocynin
KW - Contrast induced nephropathy
KW - NADPH-oxidase
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U2 - 10.1016/j.ejphar.2011.10.041
DO - 10.1016/j.ejphar.2011.10.041
M3 - Article
C2 - 22094062
AN - SCOPUS:84855555390
SN - 0014-2999
VL - 674
SP - 397
EP - 406
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 2-3
ER -