Protective effects of granulocyte colony-stimulating factor on acute hepatic failure induced by D-galactosamine/lipopolysaccharide in mice.
- Author:
Xu-wen XU
1
;
De-ming TAN
;
Meng-hou LU
Author Information
1. Institute of Infectious Diseases, Xiangya Hospital, Central South University, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Galactosamine;
Granulocyte Colony-Stimulating Factor;
therapeutic use;
Lipopolysaccharides;
Liver Failure, Acute;
chemically induced;
drug therapy;
Male;
Mice;
Protective Agents;
therapeutic use;
Random Allocation;
Recombinant Proteins
- From:
Journal of Central South University(Medical Sciences)
2006;31(4):543-547
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To evaluate the protective effect of recombinant human granulocyte colony stimulating factor (rhG-CSF) on acute hepatic failure induced by galactosamine (D-GalN) and lipopolysaccharide (LPS) in mice, and to explore its mechanism.
METHODS:The mice were intraperitoneally administered D-GalN (800 mg/kg) and LPS (10 microg/kg), and then were intraperitoneally injected either saline (the control group )or rhG-CSF at 300 microg/kg body weight (the therapy group) at 4 h, 2 h and 0 h before the D-GalN/LPS injection. The survival rate of the mice was estimated at 24 h after the D-GalN/LPS injection. The degree of hepatic injury was evaluated at 6 h after the D-GalN/LPS injection, and the levels of TNF-alpha, IFN-gamma, IL-6 and IL-10 mRNA were simultaneously measured by semiquantitative RT-PCR.
RESULTS:The survival rate of the therapy group was significantly higher than that of the control group (68.4% vs 20%, P<0.01). As compared with the control group, the degree of liver injury in the therapy group significantly decreased (P<0.05), and the levels of TNF-alpha and IFN-gamma mRNA in the hepatic tissue also reduced remarkably (P<0.01, respectively), while the levels of IL-6 and IL-10 mRNA increased (P<0.01, respectively) at 6 h after the D-GalN/LPS injection.
CONCLUSION:G-CSF can protect the mice from acute hepatic failure induced by D-GalN/LPS.
