title: The protective effect of oxytocin on renal ischemia/reperfusion injury in rats.
abstract: OBJECTIVE
  Oxytocin was previously shown to have anti-inflammatory effects in different inflammation models. The major objective of the present study was to evaluate the protective role of oxytocin (OT) in protecting the kidney against ischemia/reperfusion (I/R) injury.
  
  
  METHODS
  Male Wistar albino rats (250-300 g) were unilaterally nephrectomized, and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. OT (1 mg/kg, ip) or vehicle was administered 15 min prior to ischemia and was repeated immediately before the reperfusion period. At the end of the reperfusion period, rats were decapitated and kidney samples were taken for histological examination or determination of malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration. Creatinine and urea concentrations in blood were measured for the evaluation of renal function, while TNF-alpha and lactate dehydrogenase (LDH) levels were determined to evaluate generalized tissue damage. Formation of reactive oxygen species in renal tissue samples was monitored by chemiluminescence technique using luminol and lucigenin probes.
  
  
  RESULTS
  The results revealed that I/R injury increased (p<0.01-0.001) serum urea, creatinine, TNF-alpha and LDH levels, as well as MDA, MPO and reactive oxygen radical levels in the renal tissue, while decreasing renal GSH content. However, alterations in these biochemical and histopathological indices due to I/R injury were attenuated by OT treatment (p<0.05-0.001).
  
  
  CONCLUSIONS
  Since OT administration improved renal function and microscopic damage, along with the alleviation of oxidant tissue responses, it appears that oxytocin protects renal tissue against I/R-induced oxidative damage.
authors.affiliation: Marmara University, School of Medicine, Department of Pediatric Surgery, Istanbul, Turkey. htugtepe@yahoo.com
authors.forename: Halil
authors.initials: H
authors.lastname: Tuğtepe
authors.forename: Göksel
authors.initials: G
authors.lastname: Sener
authors.forename: Neşe Karaaslan
authors.initials: NK
authors.lastname: Biyikli
authors.forename: Meral
authors.initials: M
authors.lastname: Yüksel
authors.forename: Sule
authors.initials: S
authors.lastname: Cetinel
authors.forename: Nursal
authors.initials: N
authors.lastname: Gedik
authors.forename: Berrak C
authors.initials: BC
authors.lastname: Yeğen
mesh_terms: D000818:Animals; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000517:prevention & control*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D010121:Oxytocin / Q000627:therapeutic use*; D009195:Peroxidase / Q000378:metabolism; D020011:Protective Agents / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014508:Urea / Q000097:blood
chemical_list: D020011:Protective Agents; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D010121:Oxytocin; D014508:Urea; D003404:Creatinine; D007770:L-Lactate Dehydrogenase; D009195:Peroxidase; D005978:Glutathione