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氨氯吡咪抑制大鼠黏膜鸟氨酸脱羧酶活性和DNA合成。

Amiloride inhibits rat mucosal ornithine decarboxylase activity and DNA synthesis.

作者信息

Ulrich-Baker M G, Wang P, Fitzpatrick L, Johnson L R

机构信息

Department of Physiology and Cell Biology, University of Texas Health Science Center, Houston 77225.

出版信息

Am J Physiol. 1988 Mar;254(3 Pt 1):G408-15. doi: 10.1152/ajpgi.1988.254.3.G408.

DOI:10.1152/ajpgi.1988.254.3.G408
PMID:3348406
Abstract

Refeeding fasted rats induces a dramatic trophic response in gastrointestinal mucosa and is associated with elevations in both the rate of DNA synthesis and ornithine decarboxylase (ODC) activity. The signal for these increases is unknown. Amiloride prevents cell alkalinization by blocking Na+-H+ exchange at apical epithelial cell membranes. In study 1, rats were fasted 48 h, treated with amiloride (0.5 to 500 mg/kg), and refed for 4 h. Refeeding increased ODC activities in the jejunal mucosa (X8) and liver (X19) but not in the oxyntic gland mucosa. In the jejunum, but not the liver, the activation of ODC was completely abolished by 100 mg/kg amiloride. In study 2, the rate of DNA synthesis was determined by measuring the rate of [3H]thymidine incorporation 16 h after refeeding. Refeeding resulted in significantly increased rates of DNA synthesis (dpm.microgram DNA-1.30 min-1) over fasted levels, and amiloride at 100 mg/kg significantly reduced the elevations in the jejunum and liver. In conclusion, amiloride inhibits the postprandial increases in jejunal ODC activity and DNA synthesis in the jejunum and liver. The results indicate that 1) the Na+-H+ antiport is essential to the increased ODC activity in the jejunum and the stimulation of DNA synthesis in the jejunum and liver after a meal and 2) increases in DNA synthesis and their suppression by amiloride are not necessarily linked to ODC activity.

摘要

给禁食大鼠重新喂食会在胃肠道黏膜中引发显著的营养反应,且与DNA合成速率和鸟氨酸脱羧酶(ODC)活性升高有关。这些升高的信号尚不清楚。氨氯吡咪通过阻断顶端上皮细胞膜上的Na⁺-H⁺交换来防止细胞碱化。在研究1中,大鼠禁食48小时,用氨氯吡咪(0.5至500毫克/千克)处理,然后重新喂食4小时。重新喂食使空肠黏膜(X8)和肝脏(X19)中的ODC活性增加,但在胃腺黏膜中未增加。在空肠而非肝脏中,100毫克/千克的氨氯吡咪完全消除了ODC的激活。在研究2中,通过测量重新喂食16小时后[³H]胸苷掺入率来确定DNA合成速率。重新喂食导致DNA合成速率(每分钟每微克DNA的dpm数为1.30)比禁食水平显著增加,100毫克/千克的氨氯吡咪显著降低了空肠和肝脏中的升高水平。总之,氨氯吡咪抑制餐后空肠ODC活性的增加以及空肠和肝脏中DNA合成的增加。结果表明:1)Na⁺-H⁺逆向转运对于餐后空肠中ODC活性的增加以及空肠和肝脏中DNA合成的刺激至关重要;2)DNA合成的增加及其被氨氯吡咪的抑制不一定与ODC活性相关。

相似文献

1
Amiloride inhibits rat mucosal ornithine decarboxylase activity and DNA synthesis.氨氯吡咪抑制大鼠黏膜鸟氨酸脱羧酶活性和DNA合成。
Am J Physiol. 1988 Mar;254(3 Pt 1):G408-15. doi: 10.1152/ajpgi.1988.254.3.G408.
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Mechanism of induction of mucosal ornithine decarboxylase by food.食物诱导黏膜鸟氨酸脱羧酶的机制。
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Ornithine decarboxylase and mucosal growth in response to feeding.鸟氨酸脱羧酶与进食后的黏膜生长
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Lingual factors enhance the increase of ornithine decarboxylase activity in rat jejunal mucosa after feeding.进食后,舌因素可增强大鼠空肠黏膜中鸟氨酸脱羧酶的活性增加。
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Mucosal ornithine decarboxylase in the small intestine: localization and stimulation.小肠黏膜鸟氨酸脱羧酶:定位与刺激作用
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Secretin inhibits induction of ornithine decarboxylase activity by gastrin in duodenal mucosa and IEC-6 cells.促胰液素可抑制胃泌素对十二指肠黏膜和IEC-6细胞中鸟氨酸脱羧酶活性的诱导作用。
Am J Physiol. 1994 Aug;267(2 Pt 1):G276-84. doi: 10.1152/ajpgi.1994.267.2.G276.

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