Bile reflux due to disturbed gastric movement is a cause of spontaneous gastric ulcer in W/Wν mice
Bile reflux due to disturbed gastric movement is a cause of spontaneous gastric ulcer in W/Wν mice
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DOI：
10.1023/a:1026684425642
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发表时间：
1999-06-01
影响因子：
3.1
通讯作者：
Kohli, Y
中科院分区：
文献类型：
--
作者：
Azuma, T;Dojyo, M;Kohli, Y
c-Kit是一种受体酪氨酸激酶，由小鼠W基因座编码。W/W-v突变小鼠发生自发性胃窦溃疡，本研究的目的是探讨这些胃溃疡的发病机制，并检查两种抗溃疡药物：质子泵抑制剂（2-[4-（3-甲氧基丙氧基）-3-甲基吡啶-2-基]甲基亚磺酰基）-1H-苯并咪唑钠盐，雷贝拉唑）和粘膜保护药物（香叶基香叶基丙酮，GGA）对胃溃疡的影响。与对照组相比，雷贝拉唑（30 mg/kg体重，每天皮下注射一次，持续六周）抑制胃酸分泌显着增加了胃溃疡的形成。相反，GGA治疗（100 mg/kg体重，口服给药6周）显著抑制溃疡形成。在这些突变小鼠中观察到胆汁反流，并且它们在胃窦中没有表现出周期性的强烈收缩。提示胃窦运动障碍引起的胆汁反流是W/W-v小鼠自发性胃溃疡的一个原因。
c-Kit is a receptor tyrosine kinase, and it is encoded by the mouse W locus. Mutant W/W-v mice develop spontaneous gastric antral ulcers, The aim of the present study was to investigate the pathogenesis of these gastric ulcers and to examine the effects of two antiulcer drugs; a proton pump inhibitor (2([4-(3-methoxypropoxy)-3-methylpyridine-2-yl]methyl-sulfinyl)-1H-benzimidazole sodium salt, rabeprazole) and a mucosal protective drug (geranylgeranylacetone, GGA), on the gastric ulcers. The inhibition of the gastric acid secretion by rabeprazole (30 mg/kg body weight, subcutaneous injection once a day for six weeks) significantly increased the gastric ulcer formation compared to the controls. In contrast, the GGA treatment (100 mg/kg body weight, oral administration for six weeks) significantly inhibited the ulcer formation. Bile reflux was seen in these mutant mice, and they showed no cyclic intense contractions in the gastric antrum. These results suggest that bile reflux due to the disturbance of gastric antral movement is a cause of the spontaneous gastric ulcers in W/W-v mice.