| Project/Area Number |
14370125
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hygiene
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| Research Institution | Oita University (2004)
大分医科大学 (2002-2003) |
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Principal Investigator |
MISUMI Junichi Oita University, Faculty of Medicine, Professor, 医学部, 教授 (40109658)
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| Co-Investigator(Kenkyū-buntansha) |
AOKI Kazuo Oita University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (60201282)
工藤 政信 大分大学, 医学部, 助手 (80325703)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥13,900,000 (Direct Cost: ¥13,900,000)
Fiscal Year 2004: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2003: ¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2002: ¥7,100,000 (Direct Cost: ¥7,100,000)
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| Keywords | Hericobacter pylori / NaCl / iodine / mongolian gerbils / stomach cancer / intestinal metaplasia / P53 / G1 arrest / 高食塩摂取 / 低ヨー素摂取 |
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| Research Abstract |
Mongolian gerbils can be readily infected with H.pylori, and the resultant chronic active gastritis, peptic ulcers, and intestinal metaplasia resemble lesions appearing in humans. Mongolian gerbils infected with H.pylori are very useful for the analysis of gastric carcinogenesis.
We intended to establish an animal model of stomach carcinogenesis using H.pylori-infected Mongolian gerbils with deficency I and NaCl. A total of 170 male, 7-week-old Mongolian gerbils were used for this study.
Gerbiles were randomly assigned to eight groups : 1)only given normal feed ; 2)H.pylori infection ; 3)I deficiency ; 4)H.pylori+I deficiency ; 5)5% NaCl ; 6)H.pylori+5% NaCl ; 7)5% NaCl+I deficiency ; 8)H.pylori+5% NaCl+I deficiency. The animal were killed(2005/4/4) after 27 months of the experiment.
Histopathological changes(HE stain)
In the HP infection(group 6) with high salt, there was a evident inflammatory cell infiltration in the fundus and in HP infection(group 2) ectopic pyloric glands with a severe inflammatory cell infiltration were observed the fundic regions. In addition, the cell proliferation of the pyloric mucosa was markedly accelerated in the infected animals from groups 2 and 3. The infected animals from groups 3 and 8 revealed hyperplastic changes in the pyloric mucosa, cystic glandular dilation of the pyloric glands and erosions. Some of the pyloric glands penetrated the muscularis mucosae multifocally and extended into the submucosa. Infiltration of lymphocytes, macrophages and neutrophils was seen in the lamina proplia and submucosa with formation of lymphoid follicles. On the other hand, no abnormal findings were observed in animals from group 1, whereas a severe damage of the lamina propria mucosa with a defect of glands was found in animals from group 3.
In addition, we made Alcian Blue stain and PAS stain.
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