4-Vinyl-2,6-dimethoxyphenol (canolol) suppresses oxidative stress and gastric carcinogenesis inHelicobacter pylori-infected carcinogen-treated Mongolian gerbils


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Abstract

Oxidative stress is linked to gastric carcinogenesis because of its ability to damage DNA. Here we examined antioxidative and anti-inflammatory effects of 4-vinyl-2,6-dimethoxyphenol (canolol), a recently identified potent antioxidative compound obtained from crude canola oil, onHelicobacter (H.)pylori-induced gastritis and gastric carcinogenesis using a Mongolian gerbil model. The animals were allocated toH. pylori-infection alone (12 weeks) orH.pylori+N-methyl-N-nitrosourea (MNU) administration (52 weeks). After oral inoculation ofH. pylori, they were fed for 10 and 44 weeks with or without 0.1% canolol.H. pylori-induced gastritis, 5′-bromo-2′-deoxyuridine (BrdU) labeling and scores for cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) immunohistochemistry were attenuated in the canolol-treated groups. Expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), COX-2 and iNOS mRNA in the gastric mucosa, and serum 8-hydroxy-2′-deoxyguanosine (8-OHdG), anti-H. pyloriIgG and gastrin levels were also significantly lower in canolol-treated groups. Furthermore, the incidence of gastric adenocarcinomas was markedly reduced in theH. pylori+ MNU + canolol-treated group [15.0% (6/40)] compared to the control group [39.4% (13/33)] (p< 0.05). These data indicate canolol to be effective for suppressing inflammation, gastric epithelial cell proliferation and gastric carcinogenesis inH. pylori-infected Mongolian gerbils. Interestingly, the viableH. pyloricount was not changed by the canolol containing diet. Thus, the data point to the level of inflammation because ofH. pylorirather than the existence of the bacteria as the determining factor. Importantly, canolol appears to suppress induction of mRNAs for inflammatory cytokines.

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