Chinese medical journal · 2000
Induction of intestinal metaplasia in stomach of dogs and expression of tumor-related proteins in animal gastric mucosa lesions.
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Wang D, Fang D, Liu W
Аннотация
OBJECTIVE: To observe the development and progression of intestinal metaplasia (IM) in dog's stomach and expression of tumor-related proteins in gastric mucosa lesions.
METHODS: IM animal model was induced in stomach of Beagle dog by combining treatment of oral administration of N-methyl-N'-nito-N-nitrosoguanidine (MNNG) and ranitidine (R) with X-ray irradiation to the target organ. Expression of APC, p53, K-ras and bcl-2 gene proteins in animal gastric mucosa lesions were determined with immunohistochemical method.
RESULTS: IM animal model was successfully induced and the dynamic pathological changes were observed by means of this model. It was confirmed that the progression from normal epithelial cells to IM cells may require several stages, including superficial gastritis, chronic atrophic gastritis, slight focal IM and moderate or severe IM. Aberrant bcl-2 protein can be detected in the atrophic mucosa epithelium and the abnormal expression of APC, K-ras and bcl-2 can be found in IM of mucosa.
CONCLUSIONS: IM model in stomach of Beagle dog can be successfully induced by our method (MNNG + R + X-ray). The progression from normal to IM in dog resembles that of human being and the expression of tumor-related proteins (APC, bcl-2, K-ras) may play a role in the malignant transformation of IM.
METHODS: IM animal model was induced in stomach of Beagle dog by combining treatment of oral administration of N-methyl-N'-nito-N-nitrosoguanidine (MNNG) and ranitidine (R) with X-ray irradiation to the target organ. Expression of APC, p53, K-ras and bcl-2 gene proteins in animal gastric mucosa lesions were determined with immunohistochemical method.
RESULTS: IM animal model was successfully induced and the dynamic pathological changes were observed by means of this model. It was confirmed that the progression from normal epithelial cells to IM cells may require several stages, including superficial gastritis, chronic atrophic gastritis, slight focal IM and moderate or severe IM. Aberrant bcl-2 protein can be detected in the atrophic mucosa epithelium and the abnormal expression of APC, K-ras and bcl-2 can be found in IM of mucosa.
CONCLUSIONS: IM model in stomach of Beagle dog can be successfully induced by our method (MNNG + R + X-ray). The progression from normal to IM in dog resembles that of human being and the expression of tumor-related proteins (APC, bcl-2, K-ras) may play a role in the malignant transformation of IM.