title: Ischaemic postconditioning reduces serum and tubular TNF-α expression in ischaemic-reperfused kidney in healthy rats.
abstract: OBJECTIVE
  We studied the protective effects of postconditioning (PS) in healthy and hypercholesterolemic rats after renal ischaemia-reperfusion (IR) injury. We aimed to examine cytokine expression and apoptosis in tissue damage after revascularisation (TNF-α levels in serum and tissue).
  
  
  METHODS
  Male Wistar rats (n = 32) were divided into four groups. The animals of normal feed groups (NF) were fed with normal rat chow and the cholesterol feed groups (CF) were fed with 1.5% cholesterol containing diet for 8 weeks. Anaesthetized rats underwent a 45-min cross-clamping in both kidney pedicles. Ischaemia was followed by 120-min reperfusion with or without PS protocol (group PS vs. IR). Postconditioning was induced by four intermittent periods of ischaemia-reperfusion of 15-s duration each. Serum cholesterol, triglyceride, urea and creatinine levels were determined. Proinflammation was characterized by the measurement of serum TNF-α. Tissue injury in kidney was determined by formaline-fixed, paraffin-embedded tissue sections. Tissue TNF-α levels were determined by immunohistochemistry.
  
  
  RESULTS
  Significant elevation was observed in serum TNF-α level after IR injury in normal feed groups, which was reduced by PS. In CF group neither the elevation nor the postconditioning induced reduction were as significant as in the NF groups. In normal feed group PS caused a significant reduction in tissue TNF-α level which was significantly higher in CF.
  
  
  CONCLUSIONS
  Ischaemic postconditioning proved to be an effective defense against IR in NF groups, but it was ineffective in CF groups in kidney tissue.
authors.affiliation: Department of Surgical Research and Techniques, University of Pecs Medical School, Pecs, Hungary.
authors.forename: Z
authors.initials: Z
authors.lastname: Miklós
authors.forename: M
authors.initials: M
authors.lastname: Kürthy
authors.forename: P
authors.initials: P
authors.lastname: Degrell
authors.forename: E
authors.initials: E
authors.lastname: Ranczinger
authors.forename: M
authors.initials: M
authors.lastname: Vida
authors.forename: J
authors.initials: J
authors.lastname: Lantos
authors.forename: E
authors.initials: E
authors.lastname: Arató
authors.forename: L
authors.initials: L
authors.lastname: Sínay
authors.forename: P
authors.initials: P
authors.lastname: Hardi
authors.forename: B
authors.initials: B
authors.lastname: Balatonyi
authors.forename: S
authors.initials: S
authors.lastname: Ferencz
authors.forename: Sz
authors.initials: S
authors.lastname: Jávor
authors.forename: V
authors.initials: V
authors.lastname: Kovács
authors.forename: B
authors.initials: B
authors.lastname: Borsiczky
authors.forename: Gy
authors.initials: G
authors.lastname: Wéber
authors.forename: E
authors.initials: E
authors.lastname: Rőth
authors.forename: G
authors.initials: G
authors.lastname: Jancsó
mesh_terms: D000818:Animals; D002784:Cholesterol / Q000097:blood; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood; D007150:Immunohistochemistry; D057775:Ischemic Postconditioning / Q000379:methods*; D007668:Kidney / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000097:blood* / Q000378:metabolism / Q000473:pathology; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000097:blood* / Q000494:pharmacology
chemical_list: D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002784:Cholesterol; D003404:Creatinine