高级搜索
实验性胃粘膜肠上皮化生组织发生的研究[J]. 肿瘤防治研究, 1994, 21(3): 148-149.
引用本文: 实验性胃粘膜肠上皮化生组织发生的研究[J]. 肿瘤防治研究, 1994, 21(3): 148-149.
Histogenesis of Intestinal Metaplasia of Gastric Mucosa Induced Experimentally in Wistar Rats[J]. Cancer Research on Prevention and Treatment, 1994, 21(3): 148-149.
Citation: Histogenesis of Intestinal Metaplasia of Gastric Mucosa Induced Experimentally in Wistar Rats[J]. Cancer Research on Prevention and Treatment, 1994, 21(3): 148-149.

实验性胃粘膜肠上皮化生组织发生的研究

Histogenesis of Intestinal Metaplasia of Gastric Mucosa Induced Experimentally in Wistar Rats

  • 摘要: 本文首次报道应用小剂量MNNG和雷尼替丁诱发了Wistar鼠实验性胃粘膜肠化生,应用该模型对肠化的发生、发展过程进行动态观察。肠化最早出现于实验第9周,在第12周以前,化生只见于腺颈部;第14、16周的标本上可见肠化生自腺颈部向上或向下延伸;第18、20周及以后的标本上,可见到胃粘膜不同部位的肠化生,尤以胃粘膜下1/3最为显著。结果说明肠化生起源于胃粘膜腺颈部增殖细胞区,之后可向粘膜表面或腺底部发展,似乎以后者为主。

     

    Abstract: Histogenesis of intestinal metaplasia(IM) of gastric mucosa was studied in Wistar rats treated with N-methyl-N'-nitro-N-nitrosoguanidine(MNNG) and ranitidine.IM was found from 9 weeks after the beginning of MNNG and ranitidine administration.Metaplastic glands appeared only in neck region before 12 weeks.and followed upwards and downwards at 14 and 16 weeks.IM in the different levels of the gastric mucusa,mainly confined to the lower third of thes mucosa was observed after 18 weeks.These findings suggest that IM arise from the neek proliferative cell zone and then extend to the surface and bottom of the gastric mucosa.

     

/

返回文章
返回