Pyrrolidine dithiocarbamate reduces renal dysfunction and injury caused by ischemia/reperfusion of the rat kidney

Dithiocarbamates can modulate the expression of genes associated with inflammation or development of ischemia/reperfusion injury. Here, we investigate the effects of pyrrolidine dithiocarbamate, an inhibitor of nuclear factor (NF)-κB activation, on the renal dysfunction and injury caused by ischemia...

Full description

Saved in:
Bibliographic Details
Published in:European journal of pharmacology 2003-12, Vol.482 (1), p.271-280
Main Authors: Chatterjee, Prabal K., di Villa Bianca, Roberta D'Emmanuele, Sivarajah, Ahila, McDonald, Michelle C., Cuzzocrea, Salvatore, Thiemermann, Christoph
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Dithiocarbamates
Inducible nitric oxide synthase
Kidney - blood supply
Kidney - drug effects
Kidney - pathology
Male
Medical sciences
Nitric oxide
Nuclear factor-κB
Pharmacology. Drug treatments
Pyrrolidine dithiocarbamate
Pyrrolidines - pharmacology
Pyrrolidines - therapeutic use
Rats
Rats, Wistar
Renal/kidney
Reperfusion Injury - drug therapy
Reperfusion Injury - pathology
Reperfusion-injury
Thiocarbamates - pharmacology
Thiocarbamates - therapeutic use
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Dithiocarbamates can modulate the expression of genes associated with inflammation or development of ischemia/reperfusion injury. Here, we investigate the effects of pyrrolidine dithiocarbamate, an inhibitor of nuclear factor (NF)-κB activation, on the renal dysfunction and injury caused by ischemia/reperfusion of the rat kidney. Bilateral clamping of renal pedicles (45 min) followed by reperfusion (6 h) caused significant renal dysfunction and marked renal injury. Pyrrolidine dithiocarbamate (100 mg/kg, administered i.v.) significantly reduced biochemical and histological evidence of renal dysfunction and injury caused by ischemia/reperfusion of the rat kidney. Furthermore, pyrrolidine dithiocarbamate markedly reduced the expression of inducible nitric oxide synthase (iNOS) protein and significantly reduced serum levels of nitric oxide. Finally, pyrrolidine dithiocarbamate inhibited the activation of NF-κB by preventing its translocation from the cytoplasm into the nuclei of renal cells. These results demonstrate that pyrrolidine dithiocarbamate reduces renal ischemia/reperfusion injury and that dithiocarbamates may provide beneficial actions against ischemic acute renal failure.
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2003.09.071