title: The protective effect of nesfatin-1 against renal ischemia-reperfusion injury in rats.
abstract: BACKGROUND
  The pathogenetic mechanisms underlying ischemia-reperfusion (I/R) injury involve oxidative stress, inflammation and apoptosis. Nesfatin-1, a novel peptide, has been reported to possess antioxidant, anti-inflammatory and anti-apoptic properties. The study was to examine the potential protective effects of nesfatin-1 on renal I/R injury.
  
  
  METHODS
  I/R model was induced by placing a clamp across left renal artery for 45 min followed by 24 h reperfusion, along with a contralateral nephrectom. Twenty-four rats divided into three groups: sham-operated group, vehicle-treated I/R and nesfatin-1-treated I/R. Nesfatin-1 was intraperitoneally injected 30 min before renal ischemia. We harvested serum and kidneys at 24 h after reperfusion. Renal function and histological changes were assessed. Marker of oxidative stress and cells in kidney were also evaluated.
  
  
  RESULTS
  The animals with nesfatin-1 significantly improved renal functional and histologic lesions induced by I/R injury. The malondialdehyde (MDA) level decreased, whereas superoxide dismutase (SOD) and catalase (CAT) activities were significantly increased. Moreover, nesfatin-1-treated rats had a markedly decrease in apoptotic tubular cells, as well as a decrease in caspase-3 activity and an increase in the bcl-2/Bax ratio.
  
  
  CONCLUSIONS
  This is the first evidence that nesfatin-1 treatment ameliorates acute renal I/R injury by suppressing oxidative stress and cell apoptosis. Therefore, it is promising as a potential therapeutic agent for renal IR injury.
authors.affiliation: a Department of Urology , Renmin Hospital of Wuhan University , Wuhan , Hubei , PR China.
authors.forename: Guanjun
authors.initials: G
authors.lastname: Jiang
authors.forename: Min
authors.initials: M
authors.lastname: Wang
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.forename: Hui
authors.initials: H
authors.lastname: Chen
authors.forename: Zhiyuan
authors.initials: Z
authors.lastname: Chen
authors.forename: Jia
authors.initials: J
authors.lastname: Guo
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Weng
authors.forename: Xiuheng
authors.initials: X
authors.lastname: Liu
mesh_terms: D058186:Acute Kidney Injury / Q000473:pathology*; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D017209:Apoptosis / Q000187:drug effects; D002135:Calcium-Binding Proteins / Q000008:administration & dosage*; D053148:Caspase 3 / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000008:administration & dosage*; D007668:Kidney / Q000473:pathology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000008:administration & dosage*; D000080866:Nucleobindins; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000473:pathology*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D002135:Calcium-Binding Proteins; D004268:DNA-Binding Proteins; D009419:Nerve Tissue Proteins; C000630652:Nucb1 protein, rat; D000080866:Nucleobindins; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D053148:Caspase 3
keywords: Apoptosis; nesfatin-1; oxidative stress; renal ischemia–reperfusion injury