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Synergistic promoting effects of Helicobacter pylori infection and high-salt diet on gastric carcinogenesis in Mongolian gerbils.幽门螺杆菌感染与高盐饮食对蒙古沙鼠胃癌发生的协同促进作用。
Jpn J Cancer Res. 2002 Oct;93(10):1083-9. doi: 10.1111/j.1349-7006.2002.tb01209.x.
2
Helicobacter pylori infection enhances N-methyl-N-nitrosourea-induced stomach carcinogenesis in the Mongolian gerbil.幽门螺杆菌感染会增强N-甲基-N-亚硝基脲诱导的蒙古沙鼠胃癌发生。
Cancer Res. 1998 May 15;58(10):2067-9.
3
[Eradication model employing Mongolian gerbils treated with chemical carcinogen and infected with Helicobacter pylori--implications for human cancer prevention].[采用经化学致癌物处理并感染幽门螺杆菌的蒙古沙鼠的根除模型——对人类癌症预防的启示]
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4
Induction of glandular stomach cancers in Helicobacter pylori-sensitive Mongolian gerbils treated with N-methyl-N-nitrosourea and N-methyl-N'-nitro-N-nitrosoguanidine in drinking water.在饮用水中用N-甲基-N-亚硝基脲和N-甲基-N'-硝基-N-亚硝基胍处理对幽门螺杆菌敏感的蒙古沙鼠诱发腺胃癌。
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Role of Helicobacter pylori in gastric carcinogenesis: the origin of gastric cancers and heterotopic proliferative glands in Mongolian gerbils.幽门螺杆菌在胃癌发生中的作用:蒙古沙鼠胃癌及异位增生腺的起源
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7
Earlier Helicobacter pylori infection increases the risk for the N-methyl-N-nitrosourea-induced stomach carcinogenesis in Mongolian gerbils.早期幽门螺杆菌感染会增加蒙古沙鼠因N-甲基-N-亚硝基脲诱导的胃癌发生风险。
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8
High salt diets dose-dependently promote gastric chemical carcinogenesis in Helicobacter pylori-infected Mongolian gerbils associated with a shift in mucin production from glandular to surface mucous cells.高盐饮食以剂量依赖的方式促进幽门螺杆菌感染的蒙古沙鼠的胃化学致癌作用,这与粘蛋白产生从腺细胞向表面粘液细胞的转变有关。
Int J Cancer. 2006 Oct 1;119(7):1558-66. doi: 10.1002/ijc.21810.
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Timing of N-methyl-N-nitrosourea administration affects gastric carcinogenesis in Mongolian gerbils infected with Helicobacter pylori.N-甲基-N-亚硝基脲给药时间影响感染幽门螺杆菌的蒙古沙鼠的胃癌发生。
Cancer Lett. 2000 Nov 10;160(1):99-105. doi: 10.1016/s0304-3835(00)00571-1.
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Eradication diminishes enhancing effects of Helicobacter pylori infection on glandular stomach carcinogenesis in Mongolian gerbils.根除幽门螺杆菌可减轻其感染对蒙古沙鼠腺胃癌发生的促进作用。
Cancer Res. 2000 Mar 15;60(6):1512-4.

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Prevention of Gastric Cancer: Eradication of Helicobacter Pylori and Beyond.胃癌的预防:根除幽门螺杆菌及其他措施
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本文引用的文献

1
Reversibility of heterotopic proliferative glands in glandular stomach of Helicobacter pylori-infected Mongolian gerbils on eradication.幽门螺杆菌感染的蒙古沙鼠腺胃异位增殖性腺的根除后可逆性
Jpn J Cancer Res. 2002 Apr;93(4):374-81. doi: 10.1111/j.1349-7006.2002.tb01267.x.
2
Helicobacter pylori and two ultrastructurally distinct layers of gastric mucous cell mucins in the surface mucous gel layer.幽门螺杆菌与表面黏液凝胶层中胃黏液细胞黏蛋白的两个超微结构不同的层。
Gut. 2001 Oct;49(4):474-80. doi: 10.1136/gut.49.4.474.
3
Effects of Helicobacter pylori infection on gastric acid secretion and serum gastrin levels in Mongolian gerbils.幽门螺杆菌感染对蒙古沙鼠胃酸分泌和血清胃泌素水平的影响。
Gut. 2001 Jun;48(6):765-73. doi: 10.1136/gut.48.6.765.
4
Serum immunoglobulin G immune response to Helicobacter pylori antigens in Mongolian gerbils.蒙古沙鼠对幽门螺杆菌抗原的血清免疫球蛋白G免疫反应。
J Clin Microbiol. 2001 Apr;39(4):1283-8. doi: 10.1128/JCM.39.4.1283-1288.2001.
5
Eradication diminishes enhancing effects of Helicobacter pylori infection on glandular stomach carcinogenesis in Mongolian gerbils.根除幽门螺杆菌可减轻其感染对蒙古沙鼠腺胃癌发生的促进作用。
Cancer Res. 2000 Mar 15;60(6):1512-4.
6
Interleukin-1 polymorphisms associated with increased risk of gastric cancer.与胃癌风险增加相关的白细胞介素-1基因多态性。
Nature. 2000 Mar 23;404(6776):398-402. doi: 10.1038/35006081.
7
New animal model of glandular stomach carcinogenesis in Mongolian gerbils infected with Helicobacter pylori and treated with a chemical carcinogen.感染幽门螺杆菌并经化学致癌物处理的蒙古沙鼠腺胃癌发生新动物模型。
J Gastroenterol. 1999;34 Suppl 11:61-6.
8
High-salt diet induces gastric epithelial hyperplasia and parietal cell loss, and enhances Helicobacter pylori colonization in C57BL/6 mice.高盐饮食会诱导C57BL/6小鼠出现胃上皮增生和壁细胞丢失,并增强幽门螺杆菌的定植。
Cancer Res. 1999 Oct 1;59(19):4823-8.
9
Helicobacter pylori infection enhances glandular stomach carcinogenesis in Mongolian gerbils treated with chemical carcinogens.幽门螺杆菌感染可增强经化学致癌物处理的蒙古沙鼠腺胃癌变。
Carcinogenesis. 1999 Apr;20(4):669-76. doi: 10.1093/carcin/20.4.669.
10
Helicobacter pylori: the gastric cancer problem.幽门螺杆菌:胃癌问题
Gut. 1998 Jul;43 Suppl 1(Suppl 1):S33-4. doi: 10.1136/gut.43.2008.s33.

幽门螺杆菌感染与高盐饮食对蒙古沙鼠胃癌发生的协同促进作用。

Synergistic promoting effects of Helicobacter pylori infection and high-salt diet on gastric carcinogenesis in Mongolian gerbils.

作者信息

Nozaki Koji, Shimizu Nobuyuki, Inada Ken-ichi, Tsukamoto Tetsuya, Inoue Manami, Kumagai Toshiko, Sugiyama Atsushi, Mizoshita Tsutomu, Kaminishi Michio, Tatematsu Masae

机构信息

Division of Oncological Pathology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya, Aichi 464-8681, Japan.

出版信息

Jpn J Cancer Res. 2002 Oct;93(10):1083-9. doi: 10.1111/j.1349-7006.2002.tb01209.x.

DOI:10.1111/j.1349-7006.2002.tb01209.x
PMID:12417037
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5926881/
Abstract

Helicobacter pylori (Hp) infection and high-salt diet administration are both considered to be important factors in gastric carcinogenesis in man. To investigate the interaction of these two factors on gastric carcinogenesis, an experimental study of the carcinogenesis model was performed. Mongolian gerbils were treated with 20 ppm of N-methyl-N-nitrosourea (MNU) in their drinking water for alternate weeks for a total of 5 weeks' exposure (groups 1, 2, 3 and 4) or were maintained as controls (groups 5, 6, 7 and 8). At week 11, the animals were inoculated with Hp (groups 1, 2, 5 and 6) or the vehicle alone (groups 3, 4, 7 and 8), and after week 12, animals were fed a 10% high salt diet (groups 1, 3, 5 and 7) or the control diet (groups 2, 4, 6 and 8). At week 50, the incidence of adenocarcinomas in group 1 (32.1%, 6 well-differentiated, 2 poorly-differentiated adenocarcinomas, and one signet-ring cell carcinoma) was significantly higher than in groups 3 (0%) (P < 0.005) and 4 (0%) (P < 0.01). The incidence of adenocarcinomas in group 2 (11.8%, one well-differentiated adenocarcinoma, and one signet-ring cell carcinoma) was also higher than in groups 3 and 4. A high-salt diet enhanced the effects of Hp infection on gastric carcinogenesis, and these two factors acted synergistically to promote the development of stomach cancers. Moreover, Hp infection promoted gastric carcinomas more than the high-salt diet.

摘要

幽门螺杆菌(Hp)感染和高盐饮食均被认为是人类胃癌发生的重要因素。为研究这两个因素在胃癌发生中的相互作用,进行了致癌模型的实验研究。将蒙古沙鼠饮用水中交替添加20 ppm的N-甲基-N-亚硝基脲(MNU),共暴露5周(第1、2、3和4组),或作为对照组(第5、6、7和8组)。在第11周,给动物接种Hp(第1、2、5和6组)或仅接种载体(第3、4、7和8组),第12周后,给动物喂食10%的高盐饮食(第1、3、5和7组)或对照饮食(第2、4、6和8组)。在第50周时,第1组腺癌的发生率(32.1%,6例高分化、2例低分化腺癌和1例印戒细胞癌)显著高于第3组(0%)(P<0.005)和第4组(0%)(P<0.01)。第2组腺癌的发生率(11.8%,1例高分化腺癌和1例印戒细胞癌)也高于第3组和第4组。高盐饮食增强了Hp感染对胃癌发生的影响,这两个因素协同作用促进了胃癌的发展。此外,Hp感染比高盐饮食更易促进胃癌发生。