title: The antiproteinuric effects of green tea extract on acute cyclosporine-induced nephrotoxicity in rats.
abstract: BACKGROUND
  It has been reported that the proteinuria is an early useful marker to detect cyclosporine (CsA) nephrotoxicity. The aim of this study was to investigate the antiproteinuric effects of green tea extract (GTE) on CsA-induced acute renal injury in rats.
  
  
  METHODS
  The rats (n = 28) were divided into four groups (n = 7/group); controls intraperitoneally (IP) injected with 0.9% saline; CsA group IP injected CsA (50 mg/kg); inducible nitric oxide synthase (iNOS) inhibitor group administered in addition NG-nitro-L-arginine-methyl ester (12 mmol/L) subcutaneously and CsA-GTE group of CsA IP plus GTE (100 mg/kg) subcutaneously.
  
  
  RESULTS
  The 24-hour urine proteins were significantly increased among the CsA (22.6 ± 3.1 mg/d) compared with the control (7.1 ± 1.5 mg/d) and significantly decreased in the CsA-GTE group (8.2 ± 1.8 mg/d, P < .01). Nitric oxide production induces by CsA treatment was significantly suppressed by GTE and iNOS inhibitor. Renal tissue malondialdehyde level was significantly increased in the CsA compared with controls and significantly decreased in the CsA-GTE group. The antioxidant enzyme activities of superoxide dysmutase and catalase, which were significantly suppressed in the CsA compared with the control group, were restored in the CsA-GTE cohort.
  
  
  CONCLUSIONS
  GTE treatment of rats showed meaningful antiproteinuric effects through antioxidative activity in kidneys from CsA-induced acute renal injury.
authors.affiliation: Department of Internal Medicine, Division of Nephrology, Chosun University Hospital, Gwangju, Republic of Korea.
authors.forename: B C
authors.initials: BC
authors.lastname: Shin
authors.forename: Y E
authors.initials: YE
authors.lastname: Kwon
authors.forename: J H
authors.initials: JH
authors.lastname: Chung
authors.forename: H L
authors.initials: HL
authors.lastname: Kim
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D016572:Cyclosporine; D019610:Cytoprotection; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology*; D011507:Proteinuria / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D013662:Tea
chemical_list: D000975:Antioxidants; D004791:Enzyme Inhibitors; D010936:Plant Extracts; D013662:Tea; D009569:Nitric Oxide; D008315:Malondialdehyde; D016572:Cyclosporine; D002374:Catalase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D013482:Superoxide Dismutase; D019331:NG-Nitroarginine Methyl Ester