Potential mechanisms underlying the effect of hepatocyte growth factor on liver injury in short bowel syndrome model rats
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In brief
In brief
This rat model study investigates how hepatocyte growth factor (HGF) may protect against liver injury in short bowel syndrome by modulating autophagy and apoptosis pathways. HGF treatment reduced hepatic steatosis and inflammation, with effects mediated through caspase 9 and autophagy markers Rubicon and p62.
Written by the GCMD Library team from the article.
Abstract
Purpose
The purpose of this study was to investigate the autophagy associated with apoptosis in hepatic damage in the short bowel syndrome rat model.
Methods
SD rats underwent jugular vein catheterization for continuous total parenteral nutrition (TPN) and 90% small bowel resection. Animals were divided into two groups: TPN plus SBS (Control group) or TPN plus SBS plus intravenous administration of HGF (HGF group). On day 7, the rats were harvested, and hepatocellular injury was evaluated.
Results
In an SBS rat model, hepatic steatosis and lobular inflammation were histologically suppressed in the HGF group (p < 0.01). The expression of tumor necrosis factor-α in the HGF group tend to be higher than that in the control group (p = 0.13). The gene expression of transforming Growth Factor-β in the HGF group was suppressed compared to the control group (p < 0.01). HGF treatment may have an antiapoptotic effect via the intrinsic pathway by caspase 9. Protein expressions of Rubicon (p = 0.03) and p62 (p < 0.01) in the HGF group were found to have increased compared to those in the control group.
Conclusion
The inhibitory effect of HGF on hepatic steatosis remains unclear, and further studies focusing on the mechanisms of fat accumulation are needed.