Severity of gastritis determines glandular stomach carcinogenesis in Helicobacter pylori-infected Mongolian gerbils
Severity of gastritis determines glandular stomach carcinogenesis in Helicobacter pylori-infected Mongolian gerbils
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DOI：
10.1111/j.1349-7006.2007.00416.x
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发表时间：
2007-04-01
期刊：
影响因子：
5.7
通讯作者：
Tatematsu, Masae
中科院分区：
文献类型：
--
作者：
Cao, Xueyuan;Tsukamoto, Tetsuya;Tatematsu, Masae
幽门螺杆菌（H. pylori）感染引起慢性胃炎，并且还与胃癌有关。本研究主要关注H.幽门诱发性胃炎是癌变的决定因素。7周龄雄性长爪沙鼠接种H. pylori，然后从20-40周给予N-甲基-N-硝基脲（MNU）。在70周，然后切除胃用于H后70、58或52周的组织学检查。pylori接种（A、B和C组分别为长期、中期和短期）。腺性胃腺癌的发生率分别为65.0%（13/20）、20.0%（2/10）和23.0%（3/13）（P < 0.05）。A组胃窦及胃体部粘膜炎症细胞浸润、增生、肠上皮化生评分及BrdU标记指数均高于B、C组（P < 0.05）;幽门螺杆菌IgG滴度和胃泌素水平也显著更高沿着粘膜白细胞介素-1 β（IL-1 β）、肿瘤坏死因子-α（TNF-α）、环氧合酶-2（考克斯-2）和诱导型一氧化氮合酶（iNOS）的mRNA水平也显著更高。结果表明，H. pylori感染在胃癌发生中起重要作用，慢性炎症，尤其是细胞增殖率的增加，在H.幽门相关性致癌
Helicobacter pylori (H. pylori) infection causes chronic gastritis and is also related to gastric carcinoma. The present study focused on severity of H. pylori-induced gastritis as a determinant of carcinogenesis. Seven-week-old male Mongolian gerbils were inoculated with H. pylori at experimental weeks 0, 12, or 18, then given N-methyl-N-nitorosourea (MNU) from weeks 20-40. At week 70, stomachs were then excised for histological examination 70, 58, or 52 weeks after H. pylori inoculation, respectively (Groups A, B, and C for long-, middle-, and short-term). The respective incidences of glandular stomach adenocarcinomas were 65.0% (13/20), 20.0% (2/10), and 23.0% (3/13) (P < 0.05). Higher scores of infiltration of inflammatory cells, hyperplasia, intestinal metaplasia and mucosal bromodeoxyuridine (BrdU) labeling index in antrum and corpus mucosa, were seen in group A than B or C (P < 0.05) and serum anti-H. pylori IgG titer and gastrin levels were also significantly higher, along with mRNA levels for mucosal interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). The results demonstrated the term and severity of H. pylori infection to play important roles in gastric carcinogenesis, with essential involvement of chronic inflammation, especially increased rates of cell proliferation, in H. pylori-associated carcinogenesis.