| Morphological and pathologic changes of experimental chronic atrophic gastritis （CAG） and the regulating mechanism of protein expression in rats |
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| 作者姓名： | Wang LJ Chen SJ Chen Z Cai JT Si JM |
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| 作者单位： | WANG Liang-jing1,CHEN Shu-jie2,CHEN Zhe§2,CAI Jian-ting1,SI Jian-min2 (1Department of Gastroenterology,the Second Affiliated Hospital,School of Medicine,Zhejiang University,Hangzhou 310009,China) (2Lab of Digestive Disease,Clinical Institute,Sir Run Run Shaw Hospital,School of Medicine,Zhejiang University,Hangzhou 310016,China) |
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| 基金项目： | 浙江省科技计划;浙江省科技计划 |
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| 摘 要： | INTRODUCTION In 1998 gastrointestinal pathologists reached aconsensus on the definition of chronic atrophic gas- tritis (CAG), which was described as programmed loss of gastric gland and/or replacement by intestinal glands in gastric mucosa. CAG was recognized to be closely related with development of gastric cancer and listed as precancerous lesions in this meeting (Genta, 1998). According to Correa (1992)’s cascade of gas-tric carcinogenesis, gastric cancer was believed to develop fr…
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| 关 键 词： | 慢性萎缩性胃炎 CAG 大鼠 蛋白质表达 病理 诊断 |
| 收稿时间： | 2005-11-06 |
| 修稿时间： | 2006-04-11 |
Morphological and pathologic changes of experimental chronic atrophic gastritis (CAG) and the regulating mechanism of protein expression in rats |
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| Wang LJ,Chen SJ,Chen Z,Cai JT,Si JM.Morphological and pathologic changes of experimental chronic atrophic gastritis (CAG) and the regulating mechanism of protein expression in rats[J].Journal of Zhejiang University Science,2006,7(8):634-640. |
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| Authors: | Liang-jing Wang Shu-jie Chen Zhe Chen Jian-ting Cai Jian-min Si |
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| Institution: | (1) Department of Gastroenterology, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China;(2) Lab of Digestive Disease, Clinical Institute, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, China |
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| Abstract: | Objective: To study the pathologic change and molecular regulation in cell proliferation and apoptosis of gastric mucosa in
rats with chronic atrophic gastritis (CAG), and evaluate the possible mechanisms. Methods: Rats were administered with 60%
alcohol or 2% salicylate sodium, 20 mmol/L deoxycholate sodium and 0.1% ammonia water to establish chronic atrophic gastritis
(CAG) models. The gastric specimens were prepared for microscopic view with hematoxylin and eosin (H-E) and alcian blue (A-B)
stain. The number of infiltrated inflammatory cells, the thickness of the mucosa gland layer (μm) and the number of gastric
glands were calculated. The damage of barrier in mucosa with erosion or ulceration, and the thickness of mucin were examined
by scanned electron microscope (SEM). The levels of PGE2, EGF (epiderminal growth factor) and gastrin in the serum were measured with radioimmunoassay or ELISA method. The immunohistochemistry
method was used to observe the number of G cells, the expression of protein of EGFR (EGF receptor), C-erbB-2, p53, p16 and
bel-2 in gastric tissue. Results: Under SEM observation, the gastric mucosa was diffused erosion or ulceration and the thickness
of mucin was decreased. Compared with normal rats, the grade of inflammatory cell infiltration in CAG rats was elevated, whereas
the thickness and number of gastric gland were significantly lower (P<0.05). Compared with normal level of (0.61±0.28) μg/L, EGF in CAG (2.24±0.83) μg/L was significantly higher (P<0.05). The levels of PGE2 and gastrin in serum were significantly lower in CAG rats than that in normal rats (P<0.05). Immunohistochemistry detection showed that the number of G cell in antrum was lower in CAG group (P<0.05). Immuno-stain showed EGFR protein expression in the basal and bilateral membrane, and the cytoplasma in atrophic gastric
gland, while negative expression was observed in normal gastric epithelial cells. Positive staining of p53 and p16 protein
was localized in the nucleus of epithelial cells. The former was higher positively expressed in atrophic gland, while the
later was higher positively stained in normal gastric tissue. bel-2 protein was positively stained in the cytoplasma in atrophic
gastric gland, while very weakly stained in normal gastric tissue. Conclusion: The pathological findings in gastric gland
accorded with the Houston diagnostic criteria of antrum-predominant CAG. CAG in rats was related with the damage of barrier
in gastric mucosa and the misbalance of cell proliferation and apoptosis. There was high protein expression of oncogene, while
inhibitor of suppressor gene in CAG rats indicated high trend of carcinogenesis.
Project (No. 011103018) supported by the Science and Technology Plan of Zhejiang Province, China
The two authors contributed equally to this work |
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| Keywords: | Chronic atrophic gastritis (CAG) Rat Protein expression |
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