title: Protective effects of captopril in diabetic rats exposed to ischemia/reperfusion renal injury.
abstract: OBJECTIVE
  To investigate the potential protective effects of captopril, the angiotensin-converting enzyme inhibitor, in diabetic rats exposed to ischaemia/reperfusion (I/R) renal injury.
  
  
  METHODS
  Following successful induction of diabetes, captopril treatment (50 mg/kg/day, p.o.) was applied for 4 weeks, after which bilateral renal ischaemia was induced for 30 min followed by reperfusion for 24 h.
  
  
  RESULTS
  Captopril significantly attenuated hyperglycaemia and hypoinsulinaemia in diabetic rats, and significantly reduced the elevations of serum creatinine and aldosterone levels, and renal malondialdehyde, tumour necrosis factor-α and nitric oxide (NO), and prevented the depletion of reduced glutathione caused by I/R in diabetic rats. Histopathological renal tissue damage induced by I/R in diabetic rats was ameliorated by captopril treatment. Immunohistochemical analysis revealed that captopril significantly attenuated the reduction of insulin content in pancreatic islet β-cells, and decreased the I/R-induced expression of inducible NO synthase, nuclear factor-κB, Fas ligand and caspase-3, and increased the expression of survivin and heme oxygenase-1 in the kidney tissue of diabetic rats.
  
  
  CONCLUSIONS
  Captopril represents a potential candidate to reduce the risk of renal injury induced by ischaemia/reperfusion in type 2 diabetes.
authors.affiliation: Department of Biomedical Sciences, Pharmacology Division, College of Medicine, King Faisal University, Al-Ahsa, Saudi Arabia. amrfouad65@yahoo.com
authors.forename: Amr A
authors.initials: AA
authors.lastname: Fouad
authors.forename: Abdulruhman S
authors.initials: AS
authors.lastname: Al-Mulhim
authors.forename: Iyad
authors.initials: I
authors.lastname: Jresat
authors.forename: Mohamed A
authors.initials: MA
authors.lastname: Morsy
mesh_terms: D000450:Aldosterone / Q000097:blood / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D053148:Caspase 3 / Q000378:metabolism; D003404:Creatinine / Q000097:blood / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D053222:Fas Ligand Protein / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D006943:Hyperglycemia / Q000097:blood / Q000378:metabolism / Q000473:pathology; D007328:Insulin / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000097:blood / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D000077022:Survivin; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; C516989:Birc5 protein, rat; D053222:Fas Ligand Protein; D007328:Insulin; D008869:Microtubule-Associated Proteins; D016328:NF-kappa B; D000077022:Survivin; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D000450:Aldosterone; D008315:Malondialdehyde; D002216:Captopril; D003404:Creatinine; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D053148:Caspase 3; D005978:Glutathione