title: Curcumin treatment protects against renal ischemia and reperfusion injury-induced cardiac dysfunction and myocardial injury.
abstract: OBJECTIVE
  Renal ischemia and reperfusion (I/R) injury frequently leads to acute renal failure (ARF) and multiple-organ injury with a substantial morbidity rate. The primary cause of ARF-associated death is, however, cardiac failure instead of renal failure itself, and the pathogenesis of renal I/R-induced cardiac injury is still poorly understood. We evaluated the efficacy of curcumin pretreatment on cardioprotection.
  
  
  METHODS
  Thirty Sprague-Dawley rats were evenly divided into 3 groups of sham-operated control, renal I/R injury, and a curcumin pretreatment group. Renal ischemia was conducted by bilateral occlusions of pedicles for 45 minutes, followed by 3 hours of reperfusion. The cardiac function was assessed by the left ventricular end-systolic-pressure-volume-relation (ESPVR), systolic pressure (SP), ejection fraction (EF), and stroke volume (SV). Myocardial injury was assessed based on creatine kinase muscle brain fraction (CK-MB) and Troponin I (cTnI), and kidney injury was assessed based on blood urea nitrogen (BUN) and creatinine. We also assessed the levels of tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) in the heart tissues.
  
  
  RESULTS
  SV, EF, and SP reduced moderately during the ischemic phase with no major change in ESPVR. During reperfusion, SV, SP, and ESPVR initially increased, and then steadily decreased. Myocardial and kidney injury were marked by the increases in serum CK-MB and cTnI, and creatinine and BUN level. Curcumin pretreatment ameliorated ESPVR and attenuated injuries of both the heart and kidney resulting from I/R insult.
  
  
  CONCLUSIONS
  Curcumin pretreatment improved cardiac contractility and attenuated myocardial and renal injury through reducing inflammatory response in the kidney and heart and oxidative stress in the myocardium.
authors: Division of Cardiovascular Surgery, Cathay General Hospital, Taipei, Taiwan.
authors: T-H
authors: TH
authors: Chen
authors: Y-C
authors: YC
authors: Yang
authors: J-C
authors: JC
authors: Wang
authors: J-J
authors: JJ
authors: Wang
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001806:Blood Urea Nitrogen; D052279:Creatine Kinase, MB Form / Q000097:blood; D003404:Creatinine / Q000097:blood; D003474:Curcumin / Q000494:pharmacology*; D019610:Cytoprotection; D004195:Disease Models, Animal; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006331:Heart Diseases / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism; D007668:Kidney / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D013318:Stroke Volume / Q000187:drug effects; D019210:Troponin I / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D016277:Ventricular Function, Left / Q000187:drug effects; D017725:Ventricular Pressure / Q000187:drug effects
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D019210:Troponin I; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D003404:Creatinine; D052279:Creatine Kinase, MB Form; D003474:Curcumin