Basic Study
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World J Gastrointest Oncol. Mar 15, 2024; 16(3): 979-990
Published online Mar 15, 2024. doi: 10.4251/wjgo.v16.i3.979
Effects of Helicobacter pylori and Moluodan on the Wnt/β-catenin signaling pathway in mice with precancerous gastric cancer lesions
Yi-Mei Wang, Zheng-Wei Luo, Yu-Lin Shu, Xiu Zhou, Lin-Qing Wang, Chun-Hong Liang, Chao-Qun Wu, Chang-Ping Li
Yi-Mei Wang, Zheng-Wei Luo, Yu-Lin Shu, Xiu Zhou, Lin-Qing Wang, Chun-Hong Liang, Chao-Qun Wu, Chang-Ping Li, Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China
Author contributions: Wang YM was responsible for purchasing materials, conducting relevant experiments, and writing articles; Luo ZW was responsible for designing the experimental plan and assisting in completing the experiment and the article; Shu YL, Zhou X, and Wang LQ were responsible for assisting in completing experiments; Liang CH and Wu CQ was responsible for helping to collect data; Li CP was responsible for guiding experiments and methods and editing the article; all authors approved the final version of the article.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Southwest Medical University (Protocol No. SWMU20230818).
Conflict-of-interest statement: There is no conflicting interest about this article.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE Guidelines, and the manuscript was prepared and revised according to the ARRIVE Guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Chang-Ping Li, MM, Academic Editor, Additional Professor, Doctor, Professor, Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Street, Luzhou 646000, Sichuan Province, China. 506854209@qq.com
Received: October 11, 2023
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
ARTICLE HIGHLIGHTS
Research background

The early diagnosis of gastric cancer (GC) is difficult. It has the characteristics of high incidence rate and high mortality. Precancerous lesion is an important stage in the development of GC. Helicobacter pylori (H. pylori) is the primary risk factor of GC, Wnt/β-catenin signaling pathway is closely related to tumor development. So their relationships with precancerous lesion should be further explored in order to explore the specific mechanisms of GC occurrence and find new drugs to prevent the development of GC.

Research motivation

Constructing a dual model of H. pylori infection and precancerous lesions of GC (PLGC) in mice is rare, and we are inspired by some recent researches. Moluodan is a traditional Chinese patent medicine and commonly used to treat digestive tract diseases. It has not yet been used for the prevention and treatment of GC. We can explore its role in the prevention of GC so that to increase its broader clinical pharmacological effects.

Research objectives

Our aim is to establish a double mouse model of H. pylori infection and PLGC, and find a new traditional Chinese patent medicine that can prevent the development of GC.

Research methods

We established a dual model of H. pylori infection and PLGC in mice. After successful modeling, the mice were freely fed with Moluodan aqueous solution to achieve the goal of drug treatment. We observed the general condition of mice throughout the entire experimental period. Subsequently, the mice were killed to detect the infection rate of H. pylori, and the pathological changes of the gastric tissue were detected by gross observation and light microscopy. The expression of Wnt/β-Catenin signaling pathway, EGF and c-Myc was detected by quantitative real-time PCR (qRT-PCR) and Western blot analyses.

Research results

Mice in the H. pylori + N-methyl-N-nitrosourea (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 used to detect the expression of Wnt/β-Catenin signaling pathway, EGF and c-Myc showed that the H. pylori + MNU group had the highest expression, followed by the MNU group, Moluodan group and the control group.

Research conclusions

H. pylori can promot the expression of Wnt/β-Catenin signaling pathway, EGF and c-Myc and accelerate the malignant progression of gastric tissues; Moluodan can inhibit the expression of Wnt/β-Catenin signaling pathway, EGF and c-Myc, protect the gastric mucosa, treat H. pylori -infected gastric mucous lesions, and prevent the malignant development of gastric tissues.

Research perspectives

Moluodan has the effect of preventing the progression of PLGC, further in-depth researches can be conducted in the future to explore its deeper mechanisms of action.