Impact of hepatocyte growth factor on the colonic morphology and gut microbiome in short bowel syndrome rat model
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In brief
In brief
This preclinical study demonstrates that hepatocyte growth factor (HGF) administration in a rat model of short bowel syndrome modulates colonic tight junction proteins and reduces LPS-producing gut bacteria while downregulating inflammatory TLR4 signaling. Findings suggest HGF may enhance intestinal barrier function through microbiome-mediated mechanisms, offering potential therapeutic insights for SBS management.
- HGF administration (0.3 mg/kg/day IV) modulates tight junction proteins in distal colon of SBS rats, potentially strengthening mucosal barrier.
- HGF treatment increases beneficial Verrucomicrobiota and reduces LPS-producing bacteria in colonic microbiome after massive small bowel resection.
- TLR4 gene expression significantly decreased in distal colon with HGF, suggesting reduced inflammatory signaling in SBS model.
- HGF effects on gut barrier and microbiome are region-specific, primarily affecting distal colon rather than proximal segments.
- HGF may offer therapeutic potential for SBS by enhancing intestinal adaptation through microbiome modulation and barrier function.
Written by the GCMD Library team from the article.
Abstract
Purpose
This study aimed to investigate the impact of hepatocyte growth factor (HGF) on colonic morphology and gut microbiota in a rat model of short bowel syndrome (SBS).
Methods
SD rats underwent jugular vein catheterization for total parenteral nutrition (TPN) and 90% small bowel resection [TPN + SBS (control group) or TPN + SBS + intravenous HGF (0.3 mg/kg/day, HGF group)]. Rats were harvested on day 7. Colonic morphology, gut microflora, tight junction, and Toll-like receptor-4 (TLR4) were evaluated.
Results
No significant differences were observed in the colonic morphological assessment. No significant differences were observed in the expression of tight junction-related genes in the proximal colon. However, the claudin-1 expression tended to increase and the claudin-3 expression tended to decrease in the distal colon of the HGF group. The Verrucomicrobiota in the gut microflora of the colon tended to increase in the HGF group. The abundance of most LPS-producing microbiota was lower in the HGF group than in the control group. The gene expression of TLR4 was significantly downregulated in the distal colon of the HGF group.
Conclusion
HGF may enhance the mucus barrier through the tight junctions or gut microbiome in the distal colon.