| Title | Helicobacter pylori-mediated gastric pathogenesis is attenuated by treatment of 2-deoxyglucose and metformin |
|---|---|
| Author | Hanfu Su1, Eun-Jung Bak2, Aeryun Kim3, Kavinda Tissera4, Jeong-Heon Cha1,2*, and Sungil Jang5* |
| Address | 1Affiliated Stomatology Hospital of Guangzhou Medical University, Guangdong Engineering Research Center of Oral Restoration and Reconstruction, Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou, Guangdong 510182, P. R. China, 2Department of Oral Biology, Oral Science Research Center, BK21 PLUS Project, Yonsei University College of Dentistry, Seoul 03722, Republic of Korea, 3Department of Dental Hygiene, Gangdong University, Eumseong 27600, Republic of Korea, 4Department of Medical Laboratory Science, Faculty of Allied Health Sciences, University of Peradeniya, Peradeniya 20400, Sri Lanka, 5Department of Oral Biochemistry, School of Dentistry, Jeonbuk National University, Jeonju 54907, Republic of Korea |
| Bibliography | Journal of Microbiology, 60(8),849-858, 2022, |
| DOI | 10.1007/s12275-022-2130-z |
| Key Words | Helicobacter pylori, 2-deoxy-D-glucose, metformin, gastritis |
| Abstract | Helicobacter pylori infection causes chronic inflammation in the stomach, which is linked to the development of gastric cancer. The anti-inflammatory and anticancer effects of a glycolysis inhibitor 2-deoxyglucose (2DG) and an antidiabetic medication metformin (Met) have gotten attention. Using a Mongolian gerbil animal model, we investigated H. pylorimediated gastric pathogenesis and how this pathogenesis is influenced by 2DG and Met. Five-week-old male gerbils were infected with H. pylori strain 7.13. After 2 weeks of infection, gerbils were fed 2DG-containing food (0.03% w/w), Met-containing water (0.5% w/v), or both (Combi) for 2 (short-term) or 10 weeks (long-term). Gastric pathogenesis and host response to H. pylori infection were examined by macroscopic and histopathologic analysis of gerbils’ stomach. As a result, indicators of gastric pathogenesis by H. pylori infection including infiltration of polymorphonuclear neutrophils and lymphocytes, intestinal metaplasia, atrophy, and proliferation of gastric epithelial cells were attenuated by short-term administration of 2DG, Met, or Combi. When the infection was sustained for long-term, gastric pathogenesis in drug-treated gerbils was equivalent to that in untreated gerbils, with the exception that the infiltration of neutrophil was reduced by 2DG. Colonization of H. pylori in stomach was unaffected by both short- and long-term treatments. Our findings demonstrate that the progression of gastric pathogenesis induced by H. pylori infection can be attenuated by the shortterm individual or combinational treatment of 2DG and Met, implying that 2DG or Met could be considered as a treatment option for gastric diseases in the early stages of infection. |