title: Ecklonia cava polyphenol protects the liver against ethanol-induced injury in rats.
abstract: BACKGROUND
  The development of alcoholic liver disease is a complex process that involves both the parenchymal and non-parenchymal cells of the liver. We examined the effect of an Ecklonia cava extract on ethanol-induced liver injury.
  
  
  METHODS
  Isolated hepatocytes and hepatic stellate cells (HSCs) were incubated with ethanol. Ecklonia cava polyphenol (ECP) was added to the cultures that had been incubated with ethanol. Male Wistar rats were fed a diet that included 0.02% or 0.2% ECP or no ECP. For a period of 3 weeks, the animals were given drinking water containing 5% ethanol and were also treated with carbon tetrachloride (CCl4) (0.1 ml/kg of body weight).
  
  
  RESULTS
  In the cultured hepatocytes, the ECP treatment suppressed the ethanol-induced increase in cell death by maintaining intracellular glutathione (GSH) levels. In HSCs, ECP treatment suppressed the ethanol-induced increases in type I collagen and α-smooth muscle actin expression by maintaining intracellular levels of reactive oxygen species and GSH. We examined the effects of ECP on serum AST and ALT activity, as well as the progression of liver fibrosis in rats treated with ethanol and CCl4. ECP treatment suppressed plasma AST and ALT activities in the ethanol- and CCl4-treated rats. ECP treatment fully protected the rats against ethanol- and CCl4-induced liver injury.
  
  
  CONCLUSIONS
  ECP may be a candidate for preventing ethanol-induced liver injury.
authors.affiliation: Department of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-Ku, Osaka, 558-8585, Japan.
authors.forename: Mai
authors.initials: M
authors.lastname: Takahashi
authors.forename: Naoko
authors.initials: N
authors.lastname: Satake
authors.forename: Haruka
authors.initials: H
authors.lastname: Yamashita
authors.forename: Akiko
authors.initials: A
authors.lastname: Tamura
authors.forename: Mio
authors.initials: M
authors.lastname: Sasaki
authors.forename: Isao
authors.initials: I
authors.lastname: Matsui-Yuasa
authors.forename: Masaki
authors.initials: M
authors.lastname: Tabuchi
authors.forename: Yasumitsu
authors.initials: Y
authors.lastname: Akahoshi
authors.forename: Masaki
authors.initials: M
authors.lastname: Terada
authors.forename: Akiko
authors.initials: A
authors.lastname: Kojima-Yuasa
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D015153:Blotting, Western; D002251:Carbon Tetrachloride / Q000633:toxicity; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D002492:Central Nervous System Depressants / Q000633:toxicity*; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000517:prevention & control*; D024042:Collagen Type I / Q000378:metabolism; D000431:Ethanol / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism; D055166:Hepatic Stellate Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D022781:Hepatocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D007124:Immunoenzyme Techniques; D020901:Kava / Q000737:chemistry*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D059808:Polyphenols / Q000627:therapeutic use*; D020011:Protective Agents / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D002492:Central Nervous System Depressants; D024042:Collagen Type I; D059808:Polyphenols; D020011:Protective Agents; D017382:Reactive Oxygen Species; D000431:Ethanol; D002251:Carbon Tetrachloride; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005978:Glutathione