title: The antifibrotic drug halofuginone reduces ischemia/reperfusion-induced oxidative renal damage in rats.
abstract: OBJECTIVE
  The objective of the present study was to evaluate the protective effects of halofuginone against renal ischemia/reperfusion (I/R) injury.
  
  
  METHODS
  Male Wistar albino rats were unilaterally nephrectomized and the left renal pedicles were occluded for 45 min to induce ischemia and then reperfused for 6 h (early) or for 72 h (late). The rats were treated intraperitoneally with either halofuginone (100 μg/kg/day) or saline 30 min prior to ischemia and the dose was repeated in the late reperfusion groups. In the sham groups, rats underwent unilateral nephrectomy and were treated at similar time points. The animals were decapitated at either 6 h or 72 h of reperfusion and trunk blood and kidney samples were obtained.
  
  
  RESULTS
  I/R injury increased renal malondialdehyde levels, myeloperoxidase activity and reactive oxygen radical levels, and decreased the renal glutathione content. Halofuginone treatment was found to reduce oxidative I/R injury and improve renal function in the rat kidney, as evidenced by reduced generation of reactive oxygen species, depressed lipid peroxidation and myeloperoxidase activity, and increased glutathione levels.
  
  
  CONCLUSIONS
  The present findings demonstrate the anti-inflammatory and antioxidant effects of halofuginone in renal I/R injury, supporting its potential use where renal I/R injury is inevitable.
authors.affiliation: Department of Pediatric Surgery, Marmara University, School of Medicine, Istanbul, Turkey. kcerit@yahoo.com
authors.forename: Kıvılcım
authors.initials: K
authors.lastname: Karadeniz Cerit
authors.forename: Berna
authors.initials: B
authors.lastname: Karakoyun
authors.forename: Meral
authors.initials: M
authors.lastname: Yüksel
authors.forename: Naziye
authors.initials: N
authors.lastname: Özkan
authors.forename: Şule
authors.initials: Ş
authors.lastname: Cetinel
authors.forename: E
authors.initials: E
authors.lastname: Tolga Dağli
authors.forename: Berrak Ç
authors.initials: BÇ
authors.lastname: Yeğen
authors.forename: Halil
authors.initials: H
authors.lastname: Tuğtepe
mesh_terms: D000818:Animals; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D005355:Fibrosis / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D005978:Glutathione / Q000378:metabolism; D007674:Kidney Diseases / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D007770:L-Lactate Dehydrogenase / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009392:Nephrectomy; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D010880:Piperidines / Q000494:pharmacology*; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology*; D052999:Quinazolinones / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology
chemical_list: D010880:Piperidines; D011500:Protein Synthesis Inhibitors; D052999:Quinazolinones; D003404:Creatinine; D007770:L-Lactate Dehydrogenase; D009195:Peroxidase; D005978:Glutathione; C010176:halofuginone