Synergistic promoting effects of Helicobacter pylori infection and high-salt diet on gastric carcinogenesis in Mongolian gerbils.
Synergistic promoting effects of Helicobacter pylori infection and high-salt diet on gastric carcinogenesis in Mongolian gerbils.
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DOI：
10.1111/j.1349-7006.2002.tb01209.x
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发表时间：
2002-10
期刊：
影响因子：
--
通讯作者：
Tatematsu M
中科院分区：
文献类型：
--
作者：
Nozaki K;Shimizu N;Inada K;Tsukamoto T;Inoue M;Kumagai T;Sugiyama A;Mizoshita T;Kaminishi M;Tatematsu M
幽门螺杆菌（Helicobacter pylori，Hp）感染和高盐饮食均被认为是人类胃癌发生的重要因素，为探讨Hp感染和高盐饮食在胃癌发生中的相互作用，采用胃癌发生模型进行了实验研究。蒙古沙鼠在饮用水中加入20 ppm N-甲基-N-亚硝基脲（MNU），每隔一周给药一次，共暴露5周（第1、2、3和4组）或作为对照（第5、6、7和8组）。在第11周，动物接种Hp（第1、2、5和6组）或仅接种溶媒（第3、4、7和8组），第12周后，动物饲喂10%高盐饮食（第1、3、5和7组）或对照饮食（第2、4、6和8组）。第50周时，第1组腺癌的发生率（32.1%，6例高分化腺癌，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组中腺癌的发生率（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，促进胃癌的发展。此外，Hp感染比高盐饮食更能促进胃癌的发生。
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.
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