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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.

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。

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本文引用的文献

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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.

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