title: Naringenin ameliorates streptozotocin-induced diabetic rat renal impairment by downregulation of TGF-β1 and IL-1 via modulation of oxidative stress correlates with decreased apoptotic events.
abstract: BACKGROUND
  Naringenin, a flavonone and a nutritive antioxidant which is mostly obtained from grapefruit, orange or tomato skin, has been extensively studied due to its radical scavenging activity.
  
  
  OBJECTIVE
  The present study investigates the protective effect of naringenin on rat kidney after streptozotocin-induced diabetes.
  
  
  METHODS
  Sixty male Wistar rats were divided into six groups. Diabetes was induced by a single intraperitoneal injection of streptozotocin (50 mg/kg) in groups II, III and IV. Naringenin 5 mg/kg body weight was given to groups III and V, but 10 mg/kg was given to groups IV and VI, orally once a day for 10 weeks. After which all animals were sacrificed, and the biochemical, histopathological, immunohistochemical and apoptotic assays were conducted.
  
  
  RESULTS
  Naringenin treatment with 5 and 10 mg/kg significantly decreased (p < 0.05) the serum biochemical parameters, elevated tissue malondialdehyde levels and increased (p < 0.01) the reduced superoxide dismutase, catalase and reduced glutathione enzyme activities in the diabetic kidney. Diabetes-induced naringenin-treated groups showed an improved histology and revealed a significant reduction in apoptosis activity (7.2 ± 0.01 and 1.8 ± 0.05) and in expression of TGF-β1 (18.9 ± 3.4 and 10.2 ± 2.1) at a dose of 5 and 10 mg/kg, respectively. Similarly, in contrast to the diabetic group, a significant difference was observed in the IL-1 expression (15.68 ± 4.3) in 5 mg/kg and (9.85 ± 2.1) in 10 mg/kg naringenin-treated groups.
  
  
  CONCLUSIONS
  Naringenin acts as a protective agent in diabetic renal impairment by altering oxidative stress, modulation of cytokines expression and apoptotic events.
authors.affiliation: a Department of Pharmaceutical Technology , NSHM Knowledge Campus , Kolkata , West Bengal , India.
authors.forename: Souvik
authors.initials: S
authors.lastname: Roy
authors.affiliation: a Department of Pharmaceutical Technology , NSHM Knowledge Campus , Kolkata , West Bengal , India.
authors.forename: Faiqa
authors.initials: F
authors.lastname: Ahmed
authors.affiliation: a Department of Pharmaceutical Technology , NSHM Knowledge Campus , Kolkata , West Bengal , India.
authors.forename: Sritama
authors.initials: S
authors.lastname: Banerjee
authors.affiliation: a Department of Pharmaceutical Technology , NSHM Knowledge Campus , Kolkata , West Bengal , India.
authors.forename: Urmi
authors.initials: U
authors.lastname: Saha
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy*; D003928:Diabetic Nephropathies / Q000097:blood / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D004305:Dose-Response Relationship, Drug; D044950:Flavanones / Q000494:pharmacology*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007375:Interleukin-1 / Q000378:metabolism*; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects; D013311:Streptozocin; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D001786:Blood Glucose; D044950:Flavanones; D007004:Hypoglycemic Agents; D007375:Interleukin-1; C508962:Tgfb1 protein, rat; D053773:Transforming Growth Factor beta1; D013311:Streptozocin; C005273:naringenin
keywords: Catalase; diabetes; histopathology; immunohistochemistry; malondialdehyde; reduce glutathione; terminal dUTP nick end-labeling