title: Oxytocin alleviates oxidative renal injury in pyelonephritic rats via a neutrophil-dependent mechanism.
abstract: BACKGROUND
  Urinary tract infection (UTI) may cause inflammation of the renal parenchyma and may lead to impairment in renal function and scar formation. Oxidant injury and reactive oxygen species (ROS) have been found responsible in the pathogenesis of UTI. The neurohypophyseal hormone oxytocin (OT) facilitates wound healing and is involved in the modulation of immune and inflammatory processes. We investigated the possible therapeutic effects of OT against Escherichia coli induced pyelonephritis in rats both in the acute and chronic setting.
  
  
  METHODS
  Twenty-four Wistar rats were injected 0.1 ml solution containing E. coli ATCC 25922 10(10) colony forming units/ml into left renal medullae. Six rats were designed as sham group and were given 0.1 ml 0.9% NaCl. Pyelonephritic rats were treated with either saline or OT immediately after surgery and at daily intervals. Half of the pyelonephritic rats were decapitated at the 24th hour of E. coli infection, and the rest were followed for 7 days. Renal function tests (urea, creatinine), systemic inflammation markers [lactate dehydrogenase (LDH) and tumor necrosis factor alpha (TNF-alpha)] and renal tissue malondialdehyde (MDA) as an end product of lipid peroxidation, glutathione (GSH) as an antioxidant parameter and myeloperoxidase (MPO) as an indirect index of neutrophil infiltration were studied.
  
  
  RESULTS
  Blood urea, creatinine, and TNF-alpha levels were increased, renal tissue MDA and MPO levels were elevated and GSH levels were decreased in both of the pyelonephritic (acute and chronic) rats. All of these parameters and elevation of LDH at the late phase were all reversed to normal levels by OT treatment.
  
  
  CONCLUSIONS
  OT alleviates oxidant renal injury in pyelonephritic rats by its anti-oxidant actions and by preventing free radical damaging cascades that involves excessive infiltration of neutrophils.
authors.affiliation: Marmara University, School of Medicine, Department of Pediatric Nephrology, Istanbul, Turkey.
authors.forename: Neşe Karaaslan
authors.initials: NK
authors.lastname: Biyikli
authors.forename: Halil
authors.initials: H
authors.lastname: Tuğtepe
authors.forename: Göksel
authors.initials: G
authors.lastname: Sener
authors.forename: Ayliz
authors.initials: A
authors.lastname: Velioğlu-Oğünç
authors.forename: Sule
authors.initials: S
authors.lastname: Cetinel
authors.forename: Sükrü
authors.initials: S
authors.lastname: Midillioğlu
authors.forename: Nursal
authors.initials: N
authors.lastname: Gedik
authors.forename: Berrak C
authors.initials: BC
authors.lastname: Yeğen
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D003094:Collagen / Q000378:metabolism; D003404:Creatinine / Q000097:blood / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000166:cytology / Q000187:drug effects* / Q000473:pathology; D007677:Kidney Function Tests; D007770:L-Lactate Dehydrogenase / Q000097:blood / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D010121:Oxytocin / Q000494:pharmacology / Q000627:therapeutic use*; D011704:Pyelonephritis / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha; D014508:Urea / Q000097:blood / Q000378:metabolism
chemical_list: D000975:Antioxidants; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D010121:Oxytocin; D014508:Urea; D003094:Collagen; D003404:Creatinine; D007770:L-Lactate Dehydrogenase; D005978:Glutathione