阿司匹林促进胃酸分泌的途径与溃疡复发

目的：探讨阿司匹林促进胃酸分泌的途径及溃疡复发的机制。方法：用乙酸复制大鼠胃溃疡模型,待第25天溃疡完全愈合后,用阿司匹林诱导已愈合的溃疡复发。在模型复制后的第55天,用免疫组化方法观测了环加氧酶-1、环加氧酶-2和胃泌素（Gas）在胃黏膜中的表达,用酶联免疫吸附法测定了胃黏膜中的前列腺素E2的含量,还测定了胃液的pH、再生黏膜厚度、扩张腺体数。结果：环加氧酶-1积分光密度在模型对照组、盐水对照组和阿司匹林组中没有差异,而阿司匹林组环加氧酶-2与Gas的积分光密度高于模型对照组和盐水对照组（P〈0.01）;阿司匹林组再生黏膜扩张腺体数高于模型对照组和盐水对照组（P〈0.01）,而再生黏膜厚度、前列腺素E2含量、pH值都低于模型对照组和盐水对照组（P〈0.01）。结论：阿司匹林可能通过抑制环加氧酶的活性导致前列腺素E2生成减少,进而促进G细胞Gas的表达,引起壁细胞分泌胃酸增多,导致愈合质量下降,使溃疡复发。

The path of Aspirin promoting gastric acid secretion and ulcer recurrence

Objective：To explore the path of Aspirin promoting gastric acid secretion and mechanisms of ulcer recurrence.Methods：The model of gastric ulcers was induced with acetic acid in rats,and the ulcers had healed on 25 days after the ulcers were induced,and then the recurrence of healed ulcer was induced with Aspirin from day 25th.On day 55th the model replication,the expression of cyclooxygenase-1,cyclooxygenase-2 and gastrin were observed in gastric mucosa with immunohistochemistry methods.The content of the prostaglandin E2 in the gastric mucosa was determined with enzyme linked immunosorbent assay.The pH of gastric juice,the regenerative mucosal thickness and the number of dilated gland were detected too.Results：The integral light density of cyclooxygenase-1 had no difference among model control group,saline control group and Aspirin group;The integral light density of cyclooxygenase-2 and gastrin,the number of dilated gland in the regenerative mucosa were increased in Aspirin group compared with those of model control group and saline control group（P0.01）,The regenerative mucosal thickness,prostaglandin E2 and pH were decreased in Aspirin group compared with those of other two groups（P0.01）.Conclusion：Aspirin decreases the production of prostaglandin E2 by inhibiting cyclooxygenase activity,which promotes the expression of gastrin of G cell,and then increases the gastric acid secretion.Increasing of the gastric acid secretion results in the quality of ulcer healing to decrease,which causes the ulcer recurrence.