4-Vinyl-2,6-dimethoxyphenol (canolol) suppresses oxidative stress and gastric carcinogenesis in Helicobacter pylori-infected carcinogen-treated Mongolian gerbils
4-Vinyl-2,6-dimethoxyphenol (canolol) suppresses oxidative stress and gastric carcinogenesis in Helicobacter pylori-infected carcinogen-treated Mongolian gerbils
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DOI：
10.1002/ijc.23245
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发表时间：
2008-04-01
影响因子：
6.4
通讯作者：
Tatematsu, Masae
中科院分区：
文献类型：
--
作者：
Cao, Xueyuan;Tsukamoto, Tetsuya;Tatematsu, Masae
氧化应激与胃癌发生有关，因为它能够破坏DNA。在这里，我们研究了4-乙烯基-2，6-二甲氧基苯酚（canolol）的抗氧化和抗炎作用，这是一种最近发现的有效的抗氧化化合物，从粗菜籽油中获得，对螺杆菌（H.）幽门致胃炎和胃癌的蒙古沙鼠模型。将动物分配至H。pylori感染（12周）或H. pylori + N-甲基-N-亚硝基脲（MNU）给药（52周）。经口接种H. pylori感染后，分别用或不用0.1%卡那洛尔喂养10周和44周。H.在canolol处理组中，幽门诱导的胃炎、5 '-溴-2'-脱氧尿苷（BrdU）标记和环氧合酶-2（考克斯-2）和诱导型一氧化氮合酶（iNOS）免疫组织化学评分减弱。检测胃黏膜白细胞介素-1 β（IL-1 β）、肿瘤坏死因子-α（TNF-α）、考克斯-2和iNOS mRNA表达及血清8-羟基脱氧鸟苷（8-OHdG）、抗H. pylori IgG和胃泌素水平在canolol治疗组中也显著较低。此外，胃腺癌的发病率在H。pylori + MNU + canolol治疗组[15.0%（6/40）]与对照组[39.4%（13/33）]相比（p <0.05）。提示卡那洛尔对H.感染幽门螺杆菌的蒙古沙鼠有趣的是，可行的H.含卡那洛尔的饮食没有改变幽门螺杆菌计数。因此，这些数据表明了H.幽门螺杆菌的存在，而不是作为决定因素的细菌。重要的是，canolol似乎抑制炎症细胞因子mRNA的诱导。(c)2007 Wiley-Liss，Inc.
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, on Helicobacter (H.) pylori-induced gastritis and gastric carcinogenesis using a Mongolian gerbil model. The animals were allocated to H. pylori-infection alone (12, weeks) or H. pylori + N-methyl-N-nitrosourea (MNU) administration (52 weeks). After oral inoculation of H. 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-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), COX-2 and iNOS mRNA in the gastric mucosa, and serum 8-hydroxy-2 '-deoxyguanosine (8-OHdG), anti-H. pylori IgG and gastrin levels were also significantly lower in canolol-treated groups. Furthermore, the incidence of gastric adenocarcinomas was markedly reduced in the H. 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 epithelia] cell proliferation and gastric carcinogenesis in H. pylori-infected Mongolian gerbils. Interestingly, the viable H. pylori count was not changed by the canolol containing diet. Thus, the data point to the level of inflammation because of H. pylori rather than the existence of the bacteria as the determining factor. Importantly, canolol appears to suppress induction of mRNAs for inflammatory cytokines. (c) 2007 Wiley-Liss, Inc.