Published online Mar 15, 2024. doi: 10.4251/wjgo.v16.i3.979
Peer-review started: October 11, 2023
First decision: December 8, 2023
Revised: December 16, 2023
Accepted: January 24, 2024
Article in press: January 24, 2024
Published online: March 15, 2024
Processing time: 152 Days and 17.8 Hours
Helicobacter pylori (H. pylori) is the primary risk factor for gastric cancer (GC), the Wnt/β-Catenin signaling pathway is closely linked to tumourigenesis. GC has a high mortality rate and treatment cost, and there are no drugs to prevent the progression of gastric precancerous lesions to GC. Therefore, it is necessary to find a novel drug that is inexpensive and preventive to against GC.
To explore the effects of H. pylori and Moluodan on the Wnt/β-Catenin signaling pathway and precancerous lesions of GC (PLGC).
Mice were divided into the control, N-methyl-N-nitrosourea (MNU), H. pylori + MNU, and Moluodan groups. We first created an H. pylori infection model in the H. pylori + MNU and Moluodan groups. A PLGC model was created in the remaining three groups except for the control group. Moluodan was fed to mice in the Moloudan group ad libitum. The general condition of mice were observed during the whole experiment period. Gastric tissues of mice were grossly and microscopically examined. Through quantitative real-time PCR (qRT-PCR) and Western blotting analysis, the expression of relevant genes were detected.
Mice in the H. pylori + MNU group showed the worst performance in general condition, gastric tissue visual and microscopic observation, followed by the MNU group, Moluodan group and the control group. QRT-PCR and Western blotting analysis were used to detect the expression of relevant genes, the results showed that the H. pylori + MNU group had the highest expression, followed by the MNU group, Moluodan group and the control group.
H. pylori can activate the Wnt/β-catenin signaling pathway, thereby facilitating the development and progression of PLGC. Moluodan suppressed the activation of the Wnt/β-catenin signaling pathway, thereby decreasing the progression of PLGC.
Core Tip: Helicobacter pylori (H. pylori) is a pathological bacteria. We explored the effects of H. pylori and the traditional Chinese medicine Moluodan on the Wnt/β-Catenin signaling pathway and precancerous lesions of GC (PLGC). Our experiments successfully established a mouse model of H. pylori infection and PLGC, which serves as a reference for others. Through the gene expression assay, we concluded that H. pylori accelerates the progression of PLGC by promoting the expression of Wnt/β-Catenin signaling pathway, epidermal growth factor (EGF) and c-Myc. Meanwhile, Moluodan can repair the gastric mucosa and delay the progression of PLGC by inhibiting the Wnt/β-Catenin signaling pathway and the expression of EGF and c-Myc.