Abstract
Background: Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation, epithelial barrier dysfunction, and increased intestinal permeability. Gallic acid is a natural polyphenol with known anti-inflammatory and antioxidant properties, but its effects on intestinal barrier regulation in IBD are not fully understood.
Objectives: To evaluate the therapeutic potential of gallic acid in experimental IBD and to investigate its effects on tight junction–dependent intestinal permeability and related intracellular signaling pathways.
Methods: Colitis was induced in Wistar rats using 3% dextran sulfate sodium. Animals were treated with gallic acid (25, 50, and 100 mg/kg) or mesalamine for fourteen days. Disease activity, colon length, histopathology, intestinal permeability, tight junction protein expression, inflammatory cytokines, oxidative stress markers, and intracellular signaling pathways were assessed. Data were analyzed using one-way ANOVA with Tukey’s post hoc test.
Results: Gallic acid significantly reduced disease severity, restored colon length, and improved histological architecture in a dose-dependent manner. Treatment markedly decreased intestinal permeability, restored tight junction protein expression, suppressed pro-inflammatory cytokines and oxidative stress, and inhibited NF-κB and MAPK signaling while activating the PI3K/Akt pathway.
Conclusion: Gallic acid effectively attenuates experimental IBD by restoring intestinal barrier integrity and modulating inflammatory signaling pathways, suggesting its potential as a therapeutic agent.