Objective: Wnt signal is very important to control the gastrointestinal mucosal proliferation, but its role in the gastric mucosal proliferation after acidified ethanol injury is not clear yet, neither is the relationship with cyclooxygenase 2 (COX-2).
Methods: X-gal staining was used to measure the expression of Wnt signaling; Western blot and RT-PCR were used to measure the expression of TCF4 and β-Catenin in the gastric mucosa before and after acidified ethanol injury. We also used TOP/flash plasmid to further identify the relationship between COX-2 and Wnt signal pathway.
Results: After acidified ethanol injury, the expression of LacZ signal, β-Catenin and TCF4 increased only in the wild type mouse. The expression of β-Catenin and TCF4 protein increased about (3.52±0.52) times and (3.02±0.62) times separately, and the expression of β-Catenin and TCF4 mRNA increased about (19.85±3.63) times and (17.82±4.82) times separately. Without ethanol injury, the expression of TOP/flash plasmid was inhibited by COX-2 inhibitor (NS398) about 80% and promoted by prostaglandin E2 (PGE2) about 50%. After 1% ethanol injury, the expression of plasmid was inhibited by NS398 about 25%; on the contrary, PGE2 promoted the expression about 10%.
Conclusion: Wnt signal in gastric mucosa is activated after acidified ethanol injury. COX-2 may work through modulating Wnt signal to control the proliferation of gastric mucosa.