title: The comparative effects of perindopril and catechin on mesangial matrix and podocytes in the streptozotocin induced diabetic rats.
abstract: BACKGROUND
  Hyperglycemia and advanced glucose end substance (AGE) are responsible for excessive reactive oxygen species (ROS) production, which causes oxidative stress in diabetes mellitus. Oxidative stress and high blood pressure may cause injury and glomerulosclerosis in the kidney. End-stage kidney failure induced by glomerulosclerosis leads to microalbuminuria (Ma) in diabetic nephropathy. We investigated the effects of an angiotensin converting enzyme inhibitor (ACEI), perindopril, and an antioxidant, catechin, on podocytes and the glomerular mesangial matrix in experimental diabetic nephropathy using ultrastructural visualization and immunohistochemical staining.
  
  
  METHODS
  We compared 5 groups of male adult Wistar albino rats: a control group, an untreated diabetic group, and diabetic groups treated with perindopril, catechin, or catechin+perindopril.
  
  
  RESULTS
  Blood glucose values in all diabetic groups were significantly higher than in the control group (p < 0.001). The body weight in all diabetic groups was significantly lower than in the control group (p < 0.001, p < 0.05). The kidney weight in the catechin+perindopril-treated diabetic group was significantly lower than in the untreated diabetic group (p < 0.001). In all treated diabetic groups, Ma levels decreased significantly (p < 0.001). Mesangial matrix and podocyte damage increased in the untreated diabetic group, but the group treated with catechin+perindopril showed less damage. TGF-beta 1 immunostaining was significantly lower in the catechin-treated and perindopril-treated groups than in the untreated diabetic group (p < 0.001). Catechin was more effective than ACEI in preventing podocyte structure. Podocytes appeared to be the first cells affected in diabetes mellitus. When exposed to hyperglycemia, podocytes caused the mesangial matrix to expand.
  
  
  CONCLUSIONS
  Catechin and perindopril were more effective in preventing renal corpuscle damage when administered together.
authors.affiliation: Department of Histology and Embryology, Cerrahpasa Faculty of Medicine, Istanbul University, Turkey. Electronic address: drpelin@yahoo.com.
authors.forename: Salime Pelin
authors.initials: SP
authors.lastname: Ertürküner
authors.affiliation: Department of Histology and Embryology, Cerrahpasa Faculty of Medicine, Istanbul University, Turkey. Electronic address: basar.murat@hotmail.com.
authors.forename: Murat
authors.initials: M
authors.lastname: Başar
authors.affiliation: Department of Medical Biology, Cerrahpasa Faculty of Medicine, Istanbul University, Turkey. Electronic address: tmatem@istanbul.edu.tr.
authors.forename: Matem
authors.initials: M
authors.lastname: Tunçdemir
authors.affiliation: Department of Histology and Embryology, Cerrahpasa Faculty of Medicine, Istanbul University, Turkey. Electronic address: isseckin@istanbul.edu.tr.
authors.forename: İsmail
authors.initials: İ
authors.lastname: Seçkin
mesh_terms: D000419:Albuminuria / Q000188:drug therapy; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002392:Catechin / Q000008:administration & dosage / Q000494:pharmacology*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000473:pathology; D003928:Diabetic Nephropathies / Q000517:prevention & control*; D005920:Glomerular Mesangium / Q000187:drug effects* / Q000473:pathology / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D020913:Perindopril / Q000008:administration & dosage / Q000494:pharmacology*; D050199:Podocytes / Q000187:drug effects* / Q000473:pathology / Q000648:ultrastructure; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin; D053773:Transforming Growth Factor beta1 / Q000032:analysis
chemical_list: D001786:Blood Glucose; D053773:Transforming Growth Factor beta1; D013311:Streptozocin; D002392:Catechin; D020913:Perindopril
keywords: Catechin; Experimental diabetic nephropathy; Perindopril; Podocyte; Rat; Slit-pore; Streptozotocin; TGF-beta 1