title: Green tea extract supplementation ameliorates CCl4-induced hepatic oxidative stress, fibrosis, and acute-phase protein expression in rat.
abstract: OBJECTIVE
  We evaluated the long-term effects of green tea extract (GTE) supplementation on oxidative stress, biliary acute phase protein expression, and liver function in CCl(4)-induced chronic liver injury.
  
  
  METHODS
  We evaluated the antioxidant activity of GTE in comparison with those of vitamin C, vitamin E, and β-carotene in vitro by using an ultrasensitive chemiluminescence analyzer. Chronic liver injury was induced by intraperitoneally administering carbon tetrachloride (CCl(4)) (1 mL/kg body weight, twice weekly) to female Wistar rats for 8 weeks. The effects of low (4 mg/kg body weight per day) and high (20 mg/kg body weight per day) doses of intragastric GTE on CCl(4)-induced liver dysfunction and fibrosis were examined by measuring the bile and blood reactive oxygen species levels and biochemical parameters by using Western blot and two-dimensional polyacrylamide gel electrophoresis techniques.
  
  
  RESULTS
  GTE has greater scavenging activity against O(2)(-), H(2)O(2), and Hypochlorous acid (HOCl) in vitro than vitamin C, vitamin E, and β-carotene do. In vivo, CCl(4) markedly increased bile and blood reactive oxygen species production, lipid accumulation, number of infiltrated leukocytes, fibrosis, hepatic hydroxyproline content, and plasma alanine aminotransferase and aspartate aminotransferase activities, and reduced plasma albumin levels. Two-dimensional polyacrylamide gel electrophoresis revealed that CCl(4) increased the acute-phase expression of six biliary proteins and decreased hepatic B-cell lymphoma 2 (Bcl-2), catalase, and CuZn superoxide dismutase protein expression. GTE supplementation attenuated CCl(4)-enhanced oxidative stress, levels of biochemical parameters, pathology, and acute-phase protein secretion, and preserved antioxidant/antiapoptotic protein expression.
  
  
  CONCLUSIONS
  GTE supplementation attenuates CCl(4)-induced hepatic oxidative stress, fibrosis, acute phase protein excretion, and hepatic dysfunction via the antioxidant and antiapoptotic defense mechanisms.
authors.affiliation: Department of Internal Medicine, Kuang-Tien General Hospital, Taichung, Taiwan.
authors.forename: Guo-Dung
authors.initials: GD
authors.lastname: Hung
authors.forename: Ping-Chia
authors.initials: PC
authors.lastname: Li
authors.forename: Hsuan-Shu
authors.initials: HS
authors.lastname: Lee
authors.forename: Huei-Min
authors.initials: HM
authors.lastname: Chang
authors.forename: Chiang-Ting
authors.initials: CT
authors.lastname: Chien
authors.forename: Kuang-Lun
authors.initials: KL
authors.lastname: Lee
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D001205:Ascorbic Acid / Q000494:pharmacology; D001219:Aspartate Aminotransferases / Q000097:blood; D001646:Bile / Q000378:metabolism; D002251:Carbon Tetrachloride; D056487:Chemical and Drug Induced Liver Injury, Chronic / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D006909:Hydroxyproline / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects; D008103:Liver Cirrhosis / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology* / Q000627:therapeutic use; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013662:Tea; D014810:Vitamin E / Q000494:pharmacology; D019207:beta Carotene / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D010936:Plant Extracts; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D013662:Tea; D019207:beta Carotene; D014810:Vitamin E; D002251:Carbon Tetrachloride; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D001205:Ascorbic Acid; D006909:Hydroxyproline