title: Hepatoprotective effect and its possible mechanism of Coptidis rhizoma aqueous extract on carbon tetrachloride-induced chronic liver hepatotoxicity in rats.
abstract: BACKGROUND
  Coptidis rhizoma is traditionally used for heat-clearing and toxic-scavenging and it belongs to liver meridian in Chinese medicine practice. Clinically, Coptidis rhizoma can be used for hepatic and biliary disorders, yet details in the therapies of liver diseases and underlying mechanism(s) remain unclear. Our previous study demonstrated that Coptidis rhizoma aqueous extract (CRAE) against CCl(4)-induced acute liver damage was related to antioxidant property. In the present study, the protection of CRAE on chronic liver damage induced by carbon tetrachloride (CCl(4)) in rats and its related mechanism were explored.
  
  
  METHODS
  The CCl(4)-induced chronic liver damage model was established, and CRAE's protective effect was examined. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity, serum and liver superoxide dismutase (SOD) activity were then measured. The histological changes were observed under microscopy and then computed in numerical score. The normal or damaged cells were isolated and related signaling pathway was evaluated.
  
  
  RESULTS
  Serum AST and ALT activities were significantly decreased in rats treated with different doses of CRAE, indicating its protective effect against CCl(4)-induced chronic liver damage. Observation on serum SOD activity revealed that CRAE might act as an anti-oxidant agent against CCl(4)-induced chronic oxide stress. Histological study supported these observations. Erk1/2 inhibition may take part into CRAE's effect on preventing hepatocyte from apoptosis when exposed to oxidative stress.
  
  
  CONCLUSIONS
  CRAE showed protective effect against CCl(4)-induced chronic liver damage in rats and its potential as an agent in the treatment of chronic liver diseases by protecting hepatocyte from injury.
authors.affiliation: School of Chinese Medicine, The University of Hong Kong, Pokfulam, Hong Kong, PR China. yfeng@hku.hk
authors.forename: Yibin
authors.initials: Y
authors.lastname: Feng
authors.forename: Ning
authors.initials: N
authors.lastname: Wang
authors.forename: Xingshen
authors.initials: X
authors.lastname: Ye
authors.forename: Huangyun
authors.initials: H
authors.lastname: Li
authors.forename: Yigang
authors.initials: Y
authors.lastname: Feng
authors.forename: Fan
authors.initials: F
authors.lastname: Cheung
authors.forename: Tadashi
authors.initials: T
authors.lastname: Nagamatsu
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001219:Aspartate Aminotransferases / Q000097:blood; D002251:Carbon Tetrachloride; D053148:Caspase 3 / Q000378:metabolism; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D000089042:Coptis chinensis; D053938:DNA Fragmentation / Q000187:drug effects; D004365:Drugs, Chinese Herbal / Q000032:analysis / Q000627:therapeutic use*; D022781:Hepatocytes / Q000187:drug effects* / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D004365:Drugs, Chinese Herbal; D002251:Carbon Tetrachloride; C107393:Coptidis rhizoma extract; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D053148:Caspase 3