title: Naringin Reduces Hyperglycemia-Induced Cardiac Fibrosis by Relieving Oxidative Stress.
abstract: BACKGROUND
  Hyperglycemia promotes myocardial fibrotic lesions through upregulation of PKC and p38 in response to redox changes. The effects of naringin on hyperglycemia-induced myocardial fibrotic changes and its putative effects on PKC-β and p38 protein expression in type 1 rat model of diabetes are hereby investigated.
  
  
  METHODS
  Male Sprague-Dawley rats were divided into six groups I-VI. Groups I and II, were orally treated with distilled water {3.0 ml/kg body weight (BW)} and naringin (50 mg/kg BW), respectively. Groups III, IV, V and VI were rendered diabetic by a single intraperitoneal injection of streptozotocin (60 mg/kg, BW) and were similarly treated with subcutaneous insulin (8.0 I.U/kg BW, twice daily), naringin (50 mg/kg BW), distilled water (3.0 ml/Kg BW) and ramipril (3.0 mg/kg/BW), respectively. The animals were sacrificed after 56 days by halothane overdose; blood and heart samples removed for further analysis.
  
  
  RESULTS
  The untreated diabetic rats exhibited significantly increased oxidative stress, NADPH oxidase activity, increased cardiac fibrosis, PKC-β and p38 mitogen activated protein kinase expression compared to controls. Naringin treatment significantly ameliorated these changes in diabetic rats compared to the untreated diabetic controls.
  
  
  CONCLUSIONS
  Naringin's amelioration of myocardial fibrosis by modulating p38 and PKC-β protein expression possibly through its known antioxidant actions and may therefore be useful in retarding the progression of fibrosis in a diabetic heart.
authors.affiliation: Molecular and Clinical Pharmacology Research Laboratory, Department of Pharmacology, Discipline of Pharmaceutical Sciences, School of Health Sciences, University of KwaZulu-Natal, P.O. Box X5401, Durban, South Africa.
authors.forename: Olubunmi A
authors.initials: OA
authors.lastname: Adebiyi
authors.affiliation: Molecular and Clinical Pharmacology Research Laboratory, Department of Pharmacology, Discipline of Pharmaceutical Sciences, School of Health Sciences, University of KwaZulu-Natal, P.O. Box X5401, Durban, South Africa.
authors.forename: Oluwafeyisetan O
authors.initials: OO
authors.lastname: Adebiyi
authors.affiliation: Molecular and Clinical Pharmacology Research Laboratory, Department of Pharmacology, Discipline of Pharmaceutical Sciences, School of Health Sciences, University of KwaZulu-Natal, P.O. Box X5401, Durban, South Africa.
authors.forename: Peter M O
authors.initials: PM
authors.lastname: Owira
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism; D044950:Flavanones / Q000008:administration & dosage* / Q000494:pharmacology; D005786:Gene Expression Regulation; D007328:Insulin / Q000008:administration & dosage* / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D018384:Oxidative Stress / Q000187:drug effects*; D011493:Protein Kinase C / Q000378:metabolism; D017257:Ramipril / Q000008:administration & dosage* / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D044950:Flavanones; D007328:Insulin; D013311:Streptozocin; D011493:Protein Kinase C; D048051:p38 Mitogen-Activated Protein Kinases; D017257:Ramipril; C005274:naringin