Suppression of histidine decarboxylase activity in rat oxyntic mucosa by beraprost sodium, a prostacyclin analogue

Tetsuya Kaneko , Yukio Nagamachi , Shigeru Matsuzaki
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Abstract

Prostaglandins (PGs) affect various aspects of gastric functions. In the present study the orally administered PGI2 derivative beraprost sodium (TRK-100, I μg per kg body weight) decreased oxyntic histidine decarboxylase activity without changing serum gastrin levels. Antral pH increased 4 hr after treatment. Beraprost also decreased the pentagastrininduced histidine decarboxylase activity at the same dose. Serum levels of secretin, somatostatin and glucose, and oxyntic mucosal levels of histamine and somatostatin, showed no significant change after treatment with beraprost. These results suggest that the response of oxyntic histidine decarboxylase to gastrin is modified by one or more prostanoids including PGI2. This mechanism might play a role in gastric mucosal protection.

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前列环素类似物伯拉前列素钠对大鼠氧合黏膜组氨酸脱羧酶活性的抑制作用
前列腺素(pg)影响胃功能的各个方面。在本研究中,口服PGI2衍生物伯拉前列素钠(TRK-100,每公斤体重1 μg)可降低氧合组氨酸脱羧酶活性,但不改变血清胃泌素水平。治疗后4小时,胃窦pH值升高。在相同剂量下,Beraprost也降低了pentagastratin诱导的组氨酸脱羧酶活性。贝拉前列素治疗后血清分泌素、生长抑素和葡萄糖水平以及氧合粘膜组胺和生长抑素水平无显著变化。这些结果表明,氧合组氨酸脱羧酶对胃泌素的反应被包括PGI2在内的一种或多种前列腺素修饰。该机制可能在胃粘膜保护中起一定作用。
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