Format

Send to

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

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

Author information

1
China Pharmaceutical University, Nanjing, China. ouyu1967@163.com <ouyu1967@163.com>

Abstract

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.

PMID:
20227401
DOI:
10.1016/j.cbi.2010.03.013
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center