Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of
nuclear factor-kappaB (
NF-kappaB) and production of proinflammatory
cytokines play important roles in the pathogenesis of IBD. In this study, the effect of
vanillin (4-hydroxy-3-methoxybenzaldehyde), a potent
nuclear factor-kappaB (
NF-kappaB) inhibitor, was evaluated in mice with trinitrobenzene
sulfonic acid (TNBS)-induced
colitis.
Oral administration of
vanillin improved macroscopic and histological features of TNBS-induced
colitis in a dose-dependent manner.
Vanillin not only prevented TNBS-induced
colitis but also ameliorated the established
colitis. By in vivo
NF-kappaB bioluminescence imaging, electrophoretic mobility shift assay, and Western blot, we found that
vanillin suppressed in vivo
NF-kappaB activities through the inhibition of p65 translocation, inhibitor of
nuclear factor-kappaB(
IkappaB)-alpha phosphorylation, and
IkappaB kinase activation. Furthermore,
vanillin reduced the expressions of proinflammatory
cytokines [
interleukin (IL)-1beta,
IL-6,
interferon-gamma, and
tumor necrosis factor-alpha] and stimulated the expression of anti-inflammatory
cytokine (IL-4) in colonic tissues. In conclusion, this work identified
vanillin as an anti-inflammatory compound with the capacity to prevent and ameliorate TNBS-induced
colitis. Due to its safety,
vanillin could be a potent candidate for the treatment of IBD.