title: Celastrol protects kidney against ischemia-reperfusion-induced injury in rats.
abstract: BACKGROUND
  Ischemia-reperfusion (IR) causes various damages in renal tissues, which is exacerbated by hypoxia-induced excessive inflammation and deteriorates the prognosis of patients after kidney surgery. Celastrol is a potent inflammation inhibitor that has little toxicity. In this report, we investigated whether celastrol protects against IR-induced renal injury in rats.
  
  
  METHODS
  Renal IR injury was induced by occlusion of the bilateral renal pedicles for 45 min followed by reperfusion for 6 h. Celastrol or vehicle solution was intraperitoneally injected 30 min before renal ischemia, respectively. Renal histology, function, and pro-inflammatory cytokines and mediators were assessed. The effect of celastrol on nuclear translocation of nuclear factor kappa B (NF-κB) was also measured.
  
  
  RESULTS
  Celastrol significantly suppressed elevation of the renal function markers and the lipid peroxidation level, alleviated renal tubular damage, and decreased the levels of tumor necrosis factor-α, interleukin-1β, and monocyte chemotactic protein-1 (MCP-1) messenger RNA in kidney caused by IR. Moreover, celastrol prevented IR-induced expression of pro-inflammatory mediators, which was associated with suppression of nuclear translocation of NF-κB subunit p65.
  
  
  CONCLUSIONS
  Celastrol ameliorated the acute kidney injury caused by IR, which was associated with inhibiting local NF-κB activation and inflammation. Our findings suggest that celastrol could be useful for preventing IR-induced renal injury.
authors: Department of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
authors: Changbin
authors: C
authors: Chu
authors: Weiyang
authors: W
authors: He
authors: Youlin
authors: Y
authors: Kuang
authors: Ke
authors: K
authors: Ren
authors: Xin
authors: X
authors: Gou
mesh_terms: D000818:Animals; D051546:Cyclooxygenase 2 / Q000032:analysis; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D007668:Kidney / Q000098:blood supply*; D008297:Male; D052247:Nitric Oxide Synthase Type II / Q000032:analysis; D053978:Pentacyclic Triterpenes; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*; D014315:Triterpenes / Q000627:therapeutic use*
chemical_list: D053978:Pentacyclic Triterpenes; D014315:Triterpenes; D018799:Intercellular Adhesion Molecule-1; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; C050414:celastrol
keywords: Celastrol; Inflammation; NF-κB; Renal ischemia–reperfusion