title: Renoprotective activity of telmisartan versus pioglitazone on ischemia/reperfusion induced renal damage in diabetic rats.
abstract: OBJECTIVE
  Diabetes mellitus (DM) causes organ dysfunction and increases the sensitivity of organs to damages.To test this hypothesis, we used renal ischemia/reperfusion (I/R) experiment to evaluate the renoprotective activity of telmisartan versus pioglitazone on I/R induced renal damage in diabetic rats.
  
  
  METHODS
  Renal I/R was performed in both normal and diabetic rats. The protocol comprised ischemia for 45 minutes followed by the reperfusion for 24 hours and a treatment period of two weeks before induction of ischemia.
  
  
  RESULTS
  Renal I/R in both control and diabetic rats induced marked renal dysfunction associated with a significant increase in the arterial pressure, tumor necrosis factor alpha (TNF-alpha) levels, and the malondialdehyde formation (MDA). The activities of the anti-oxidant enzymes such as reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were found to be decreased significantly compared to control rats. Diabetic animals that underwent renal I/R exhibited a significant increase in all the studied parameters with a reduction in the anti-oxidant enzymes as compared to non-diabetic rats. Histo-pathological studies confirm these results. Treatment with pioglitazone or telmisartan demonstrated a significant improvement in the reperfusion-induced renal injury in comparison with diabetic I/R group, without difference between the two treated groups. Therefore, the treatment with pioglitazone or telmisartan have the same corrective effect.
  
  
  CONCLUSIONS
  Type 2 diabetes had exaggerated renal I/R injury in STZ-NAD induced diabetes. Telmisartan treatment is equieffective as pioglitazone in attenuating acute I/R-induced renal injury in diabetic rats by a modification in the oxidative stress and the inflammation.
authors: Department of Pharmacology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt. dmon_kamal@yahoo.com
authors: Mona K
authors: MK
authors: Tawfik
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology*; D001565:Benzoates / Q000494:pharmacology*; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D005978:Glutathione / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000097:blood; D007668:Kidney / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008054:Lipid Peroxides / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D000077205:Pioglitazone; D051381:Rats; D015427:Reperfusion Injury / Q000097:blood / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D000077333:Telmisartan; D045162:Thiazolidinediones / Q000494:pharmacology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001565:Benzoates; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D018836:Inflammation Mediators; D008054:Lipid Peroxides; D045162:Thiazolidinediones; D014409:Tumor Necrosis Factor-alpha; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione; D000077333:Telmisartan; D000077205:Pioglitazone