Alterations in gastrin cells induced by short-term omeprazole treatment in the rat antrum: an immunocytochemical and in situ hybridization study

Abstract

Gastrin is a hormonal regulator of gastric acid secretion and a trophic stimulant of acid-producing gastric mucosa. The blockage of acid secretion has been reported to cause hypergastrinaemia and gastrin cell hyperplasia. These findings suggest that achlorhydria may stimulate gastrin gene expression in gastrin cells. In this study, we aimed to determine the alterations of gastrin mRNA by non-radioactive in situ hybridization, and also to compare the localization of transcripts and protein products of the same gene by immunocytochemistry in an acid inhibition environment provided by omeprazole. Female Sprague--Dawley rats, weighing 200--250 g, were divided into three groups. The first group was the control group (eight rats). The second group (eight rats) was given 20 mg kg−1 day−1 omeprazole as intragastric instillations for 4 days. The third group (eight rats) was given 100 mg kg−1 day−1 omeprazole as in the second group. Serum gastrin levels in the two groups treated with omeprazole showed a statistically significant increase (P < 0.001) compared with the control group. The omeprazole-treated groups also showed an increase in the number of immunoreactive gastrin cells in the pyloric mucosa and an enhancement in the intensity of immunoreaction. Cells containing gastrin mRNA signals were observed in the upper regions of the pyloric glands in the pyloric sections of the control group and in both experimental groups