Effect of ferulic acid on Wnt/β-catenin signal pathway in mice with gastritis induced by Helicobacter pylori
Objective To evaluate the effect of ferulic acid(FA)on the Wnt/β-catenin signal pathway in mice with Helicobacter pylori-induced gastritis.Methods Gastritis model in C57BL/6 mice was prepared by a combination of H.pylori infection and MNNG inducement.Then mice with gastritis were divided at random into model group,FA high and low dose groups and positive group(bismuth potassium citrate+omeprazole+clarithromycin+amoxicillin).The normal group of mice was set up at the same time.After four weeks of oral administration of medicines,the H.pylori colonization in mice were evaluated by rapid urase test.The ELISA experiments were carried out to measure the TNF-α and IL-8 levels in sera of mice.The protein expression of Wnt2 andβ-catenin in gastric mucosa were determined by immunohistochemical test.Results The H.pylori colonization rate was 100%in the model group.Comparing with that of model group,H.pylori eradication rates in groups treated with high and low doses of FA were evidently increased to 67%and 64%,respectively(P<0.01).FA(100 and 50 mg·kg1)evidently decreased the serum TNF-α and IL-8 contents of the gastritis animals,and the differences were statistically significant when compared with those of the model group(P<0.01).High and low doses of FA significantly reduced the protein expression of Wnt2 and β-catenin in gastric mucosa of mice with gastritis comparing with those of model group(P<0.01).Conclusion FA could alleviate the degree of H.pylori colonization,relieve the inflammatory reaction and prevent the epithelial-mesenchymal transition,showing a protective effect on gastric mucosa in mice with H.pylori-induced gastritis.The prevention of abnormal activation of Wnt/β-catenin signal pathway and inhibition of inflammatory cytokines expression may explain the mechanisms of FA in treating gastritis.
ferulic acidHelicobacter pylorigastritisWnt/β-catenin signal pathwayinflammatory cytokines