The administration of hepatocyte growth factor prevents total parenteral nutrition-induced hepatocellular injury in a rat model
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In brief
In brief
This rat model study demonstrates that intravenous hepatocyte growth factor (HGF) administration dose-dependently prevents TPN-induced liver injury by reducing hepatic steatosis and apoptosis. HGF shows promise as a therapeutic intervention for parenteral nutrition-associated liver disease in patients requiring long-term TPN.
Written by the GCMD Library team from the article.
Abstract
Purpose
Total parenteral nutrition (TPN) sometimes induces parenteral nutrition-associated liver disease (PNALD). Hepatocyte growth factor (HGF) acts as a potent hepatocyte mitogen anti-inflammatory and antioxidant actions. We aimed to evaluate the effect of HGF on PNALD in a rat model of TPN.
Methods
A catheter was placed in the right jugular vein for 7-day continuous TPN. All rats were divided into three groups: TPN alone (TPN group), TPN plus intravenous HGF at 0.3 mg/kg/day [TPN + HGF (low) group], and TPN plus HGF at 1.0 mg/kg/day [TPN + HGF (high) group]. On day 7, livers were harvested and the histology, inflammatory cytokines and apoptosis were evaluated.
Results
Histologically, lipid droplets were apparent in the TPN group, but decreased in the TPN + HGF (low) and TPN + HGF (high) groups. The histological nonalcoholic fatty liver disease activity scores in the TPN + HGF (low) and TPN + HGF (high) groups were significantly lower than that in the TPN group (p < 0.01). There were no significant differences in the inflammatory cytokine levels of the three groups. The caspase-9 expression levels in the TPN + HGF (low) and TPN + HGF (high) groups were significantly decreased in comparison to that in the control group (p < 0.05).
Conclusion
The intravenous administration of HGF attenuated hepatic steatosis induced by 7-day TPN dose dependently.