title: Osthole ameliorates renal ischemia-reperfusion injury by inhibiting inflammatory response.
abstract: BACKGROUND
  Renal ischemia-reperfusion (I/R) injury is a primary cause of acute renal failure that results in high mortality. This study aimed to investigate the effect of osthole, a natural coumarin derivative, on renal I/R injury in a rat model.
  
  
  METHODS
  Rats were randomly allocated to the sham operation + vehicle, I/R + vehicle, and I/R + osthole groups. Renal I/R injury was induced by clamping the left renal artery for 45 min followed by 12 h of reperfusion and a contralateral nephrectomy. Osthole (40 mg/kg) was intraperitoneally injected 30 min before inducing I/R. Renal function and histological damage were determined subsequently. Myeloperoxidase activity, monocyte/macrophage infiltration, as well as tumor necrosis factor-α, IL-1β, and activated p38 mitogen-activated protein kinase expression in kidneys were also assessed.
  
  
  RESULTS
  Osthole treatment significantly ameliorated I/R-induced renal functional and morphological injuries. Moreover, osthole treatment attenuated myeloperoxidase activity, monocyte/macrophage infiltration, and tumor necrosis factor-α, IL-1β, and activated p38 mitogen-activated protein kinase expression in kidneys.
  
  
  CONCLUSIONS
  Osthole treatment ameliorates renal I/R injury by inhibiting inflammatory responses in kidneys. Thus, osthole may represent a novel practical strategy to prevent renal I/R injury.
authors.affiliation: Department of Urology, Peking University Third Hospital, Beijing, PR China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Zheng
authors.forename: Min
authors.initials: M
authors.lastname: Lu
authors.forename: Lulin
authors.initials: L
authors.lastname: Ma
authors.forename: Shudong
authors.initials: S
authors.lastname: Zhang
authors.forename: Min
authors.initials: M
authors.lastname: Qiu
authors.forename: Xin
authors.initials: X
authors.lastname: Ma
mesh_terms: D058186:Acute Kidney Injury / Q000517:prevention & control; D000818:Animals; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D003374:Coumarins / Q000627:therapeutic use*; D004195:Disease Models, Animal; D015971:Gene Expression Regulation, Enzymologic; D007249:Inflammation / Q000517:prevention & control*; D053583:Interleukin-1beta / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D009000:Monocytes / Q000166:cytology; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D002121:Calcium Channel Blockers; D003374:Coumarins; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase; D048051:p38 Mitogen-Activated Protein Kinases; C046627:osthol