title: Therapeutic efficacy of naringin on cyclosporine (A) induced nephrotoxicity in rats: involvement of hemeoxygenase-1.
abstract: BACKGROUND
  Clinically, chronic nephrotoxicity may lead to renal functional impairment and progress to end stage renal failure. The renoprotective effect of a flavonoid naringin (NG) against cyclosporine A (CsA)-induced nephrotoxicitywas investigated in this study.
  
  
  METHODS
  Nephrotoxicity was induced in male albino Wistar rats by injecting 25 mg/kg body weight of CsAfor a period of 21 days. CsA-induced rats were also cotreated with 40 mg of NG/kg body weight, orally.
  
  
  RESULTS
  After the experimental period, the levels of lipid peroxides (TBARS) and hydroxyl radical (OH·) were found to be elevated, whereas the levels of SOD, catalase, glutathione, vitamin C, E and A were decreased in CsA-induced rats. NG co-treatment significantly decreased the levels of lipid peroxides and hydroxyl radicals and restored the levels of enzymic and non-enzymic antioxidants in renal tissues. Histological analysis revealed that CsA administration caused severe and widespread necrosis with dilatation of proximal tubules, vacuolization, tubular cell desquamation and intraluminal cast formation with massive infiltration of inflammatory cells. CsA-induced histopathological renal changes were minimal in animals which received NG treatment. The western blot and confocal microscopic expression of heme oxygenase-1 was restored by NG. In CsA-induced animals the expression was reduced compared to NG treated animals.
  
  
  CONCLUSIONS
  The present study reveals that NG can act as effective renoprotective drug against CsA-induced toxicity.
authors.affiliation: Post-Graduate Department of Biochemistry, Bharathi Women's College (Autonomous), Prakasam Salai, North Chennai 600 108, Tamil Nadu, India. csparameswari@gmail.com.
authors.forename: Yamini
authors.initials: Y
authors.lastname: Chandramohan
authors.forename: Chetenchery Somasundaram
authors.initials: CS
authors.lastname: Parameswari
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D016572:Cyclosporine; D019610:Cytoprotection; D004195:Disease Models, Animal; D044950:Flavanones / Q000494:pharmacology*; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism*; D017665:Hydroxyl Radical / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors; D014801:Vitamin A / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism
chemical_list: D000975:Antioxidants; D044950:Flavanones; D017392:Thiobarbituric Acid Reactive Substances; D014801:Vitamin A; D014810:Vitamin E; D017665:Hydroxyl Radical; D016572:Cyclosporine; D002374:Catalase; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D013482:Superoxide Dismutase; C005274:naringin; D001205:Ascorbic Acid