Tsujii M, Kawano S, Tsuji S, Ito T, Nagano K, Sasaki Y, Hayashi N, Fusamoto H, Kamada T
Department of Medicine, Osaka University Medical School, Japan.
Gastroenterology. 1993 Mar;104(3):796-801. doi: 10.1016/0016-5085(93)91015-a.
Helicobacter pylori produces ammonia in the stomach from urea. The present study was undertaken to clarify whether ammonia has an etiological role in H. pylori-associated gastric mucosal atrophy.
Ammonia at 0.01% was administered as drinking water for 8 weeks and mucosal cell migration rate and cell proliferation were investigated in rat stomach.
Long-term administration of 0.01% ammonia for 4-8 weeks decreased mucosal thickness in the antrum but not in the body. Acceleration of cell migration preceded the occurrence of mucosal atrophy. Labeling indices in both antral and body mucosa significantly increased in all ammonia-treated groups, compared with those of the control group. In the antrum, the proliferative zone was significantly enlarged as mucosal atrophy developed, whereas, in body mucosa, enlargement of the proliferative zone occurred despite the absence of mucosal atrophy.
Ammonia at 0.01% accelerates epithelial migration, especially in the antrum, leading to mucosal atrophy. Acceleration of epithelial proliferation occurs during the development of mucosal atrophy.
幽门螺杆菌可利用尿素在胃内产生氨。本研究旨在阐明氨在幽门螺杆菌相关胃黏膜萎缩中是否具有病因学作用。
将0.01%的氨作为饮用水给予大鼠8周，研究大鼠胃黏膜细胞迁移率和细胞增殖情况。
长期给予0.01%的氨4 - 8周可使胃窦部黏膜厚度降低，但胃体部未降低。细胞迁移加速先于黏膜萎缩的发生。与对照组相比，所有氨处理组的胃窦和胃体黏膜标记指数均显著增加。在胃窦部，随着黏膜萎缩的发展，增殖区显著扩大；而在胃体黏膜，尽管没有黏膜萎缩，增殖区仍发生了扩大。
0.01%的氨可加速上皮细胞迁移，尤其是在胃窦部，导致黏膜萎缩。上皮细胞增殖加速发生在黏膜萎缩发展过程中。
