Prevention of carbon tetrachloride-induced rat liver injury by soluble tumor necrosis factor receptor
MJ Czaja, J Xu, E Alt - Gastroenterology, 1995 - Elsevier
MJ Czaja, J Xu, E Alt
Gastroenterology, 1995•ElsevierBackground/Aims: Considerable indirect evidence suggests that cytokine tumor necrosis
factor α contributes to the hepatocellular damage caused by toxic liver injury. The effects of
tumor necrosis factor α neutralization on liver cell injury were determined in an in vivo model
of toxic liver injury. Methods: The in vivo effects of tumor necrosis factor α were examined in
carbon tetrachloride liver injury through the administration of a soluble tumor necrosis factor
receptor to neutralize the effects of this cytokine. Results: Soluble tumor necrosis factor …
factor α contributes to the hepatocellular damage caused by toxic liver injury. The effects of
tumor necrosis factor α neutralization on liver cell injury were determined in an in vivo model
of toxic liver injury. Methods: The in vivo effects of tumor necrosis factor α were examined in
carbon tetrachloride liver injury through the administration of a soluble tumor necrosis factor
receptor to neutralize the effects of this cytokine. Results: Soluble tumor necrosis factor …
Background/Aims
Considerable indirect evidence suggests that cytokine tumor necrosis factor α contributes to the hepatocellular damage caused by toxic liver injury. The effects of tumor necrosis factor α neutralization on liver cell injury were determined in an in vivo model of toxic liver injury.
Methods
The in vivo effects of tumor necrosis factor α were examined in carbon tetrachloride liver injury through the administration of a soluble tumor necrosis factor receptor to neutralize the effects of this cytokine.
Results
Soluble tumor necrosis factor receptor treatment decreased the degree of liver injury as measured by reduced levels of serum liver enzymes and improved histology. Soluble tumor necrosis factor receptor administration also lowered the mortality from a lethal dose of carbon tetrachloride from 60% to 16%. Tumor necrosis factor α neutralization had no detrimental effect on liver regeneration as determined by the timing of histone gene expression and postinjury liver weight.
Conclusions
These data provide direct evidence for a role of tumor necrosis factor α in toxin-induced liver cell injury. In addition, these investigations suggest that soluble tumor necrosis factor receptor therapy may be of benefit in the treatment of human liver disease.
Elsevier
