Protective effect of C-phycocyanin against carbon tetrachloride-induced hepatocyte damage in vitro and in vivo

Chem Biol Interact. 2010 Apr 29;185(2):94-100. doi: 10.1016/j.cbi.2010.03.013. Epub 2010 Mar 12.


This study focused on the hepatoprotective activity of C-phycocyanin (C-PC) against carbon tetrachloride-induced hepatocyte damage in vitro and in vivo. In in vitro study, human hepatocyte cell line L02 was used. C-PC showed its capability to reverse CCl(4)-induced L02 cells viability loss, alanine transaminase (ALT) leakage and morphological changes. C-PC also showed the following positive effects: prevent the CCl(4)-induced overproduction of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA); prevent changes in superoxide dismutase (SOD) activity; and reduce glutathione (GSH) level. In vivo, C-PC showed its capability to decrease serum ALT and aspartate transaminase (AST) levels in CCl(4)-induced liver damage in mice. The histological observations supported the results obtained from serum enzymes assays. C-PC also showed the following effects in mice liver: prevent the CCl(4)-induced MDA formation and GSH depletion; prevent SOD and glutathione peroxidase (GSH-Px) activity; and prevent the elevation of transforming growth factor-beta1 (TGF-beta1) and hepatocyte growth factor (HGF) mRNAs. Both the in vitro and in vivo results suggested that C-PC was useful in protecting against CCl(4)-induced hepatocyte damage. One of the mechanisms is believed to be through C-PCs scavenging ability to protect the hepatocytes from free radicals damage induced by CCl(4). In addition, C-PC may be able to block inflammatory infiltration through its anti-inflammatory activities by inhibiting TGF-beta1 and HGF expression.

MeSH terms

  • Alanine Transaminase / genetics
  • Alanine Transaminase / metabolism
  • Animals
  • Carbon Tetrachloride / toxicity*
  • Carbon Tetrachloride Poisoning / drug therapy
  • Carbon Tetrachloride Poisoning / prevention & control*
  • Cell Line
  • Cell Survival
  • Chemical and Drug Induced Liver Injury / enzymology
  • Chemical and Drug Induced Liver Injury / metabolism
  • Chemical and Drug Induced Liver Injury / pathology
  • Chemical and Drug Induced Liver Injury / prevention & control*
  • Glutathione Peroxidase / metabolism
  • Hepatocyte Growth Factor / antagonists & inhibitors
  • Hepatocyte Growth Factor / genetics
  • Hepatocyte Growth Factor / metabolism
  • Hepatocytes / drug effects*
  • Hepatocytes / enzymology
  • Hepatocytes / metabolism
  • Hepatocytes / pathology
  • Humans
  • Malondialdehyde / metabolism
  • Mice
  • Mice, Inbred ICR
  • Microscopy, Fluorescence
  • Phycocyanin / pharmacology*
  • Phycocyanin / therapeutic use
  • Protective Agents / pharmacology*
  • Protective Agents / therapeutic use
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reactive Oxygen Species / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Superoxide Dismutase / metabolism
  • Transforming Growth Factor beta1 / antagonists & inhibitors
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism


  • Protective Agents
  • RNA, Messenger
  • Reactive Oxygen Species
  • Transforming Growth Factor beta1
  • Phycocyanin
  • Malondialdehyde
  • Hepatocyte Growth Factor
  • Carbon Tetrachloride
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Alanine Transaminase