Dietary approaches to preventing Helicobacter pylori (H. pylori)-associated gastric
carcinogenesis are widely accepted because surrounding break-up mechanisms are mandatory for
cancer prevention, however, eradication alone has been proven to be insufficient. Among these dietary interventions, omega-3-polyunsaturated-fatty
acids (ω-3 PUFAs) are often the first candidate selected. However, there was no trial of
fatty acids in preventing H. pylori-associated
carcinogenesis and inconclusive results have been reported, likely based on inconsistent dietary administration. In this study, we developed an H. pylori initiated-, high
salt diet promoted-gastric
tumorigenesis model and conducted a comparison between wild-type (WT) and Fat-1-transgenic (TG)-mice. Gross and pathological lesions in mouse stomachs were evaluated at 16, 24, 32, and 45 weeks after H. pylori
infection, and the underlying molecular changes to explain the
cancer preventive effects were investigated. Significant changes in: i) ameliorated gastric
inflammations at 16 weeks of H. pylori
infection, ii) decreased angiogenic
growth factors at 24 weeks, iii) attenuated
atrophic gastritis and
tumorigenesis at 32 weeks, and iv) decreased
gastric cancer at 45 weeks were all noted in Fat-1-TG-mice compared to WT-mice. While an increase in the expression of
Cyclooxygenase (COX)-2, and reduced expression of the
tumor suppressive 15-PGDH were observed in WT-mice throughout the experimental periods, the expression of
Hydroxyprostaglandin dehydrogenase (15-PGDH) was preserved in Fat-1-TG-mice. Using a comparative
protein array, attenuated expressions of
proteins implicated in proliferation and
inflammation were observed in Fat-1-TG-mice compared to WT-mice. Conclusively, long-term administration of ω-3 PUFAs can suppress H. pylori-induced gastric
tumorigenesis through a dampening of
inflammation and reduced proliferation in accordance with afforded
rejuvenation.