Ultrastructural intestinal mucosa change after prolonged inhibition of gastric acid secretion by omeprazole in male rats
- PDF / 25,303,511 Bytes
- 15 Pages / 595.276 x 790.866 pts Page_size
- 48 Downloads / 177 Views
ORIGINAL ARTICLE
Ultrastructural intestinal mucosa change after prolonged inhibition of gastric acid secretion by omeprazole in male rats Siriporn Chamniansawat1 · Nattida Kampuang2 · Nasisorn Suksridechacin2 · Narongrit Thongon2 Received: 11 June 2020 / Accepted: 2 September 2020 © Japanese Association of Anatomists 2020
Abstract Omeprazole is a potent inhibitor of gastric acid secretion. It was reported that omeprazole induced dramatic gastric mucosa morphologic changes from the resting state to the stimulated state. However, the effect of omeprazole administration on the ultrastructure and absorptive function of small intestines was largely unknown. Here, male Sprague–Dawley rats were daily treated with a single dose of omeprazole for 12 or 24 weeks. Ultrastructure intestinal mucosal change in duodenum, jejunum, and ileum was observed. We also determined small intestine inflammation, using intraepithelial lymphocytes activation. Finally, magnesium levels were measured in plasma, urine, feces, muscle, and bone to determine systemic magnesium balance. Omeprazole-treated rats had significantly decreased the width of tight junction, villous length, and absorptive area of duodenum, jejunum, and ileum compared to control rats. The small intestine of the omeprazole-treated group showed significantly higher intraepithelial lymphocytes activation levels compared with the control group. Lower secretory granules of Paneth cells at the base of the crypts were showed in omeprazole-treated rats. They also had significantly lower plasma, urinary, bone, and muscle Mg2+ contents indicating hypomagnesemia with systemic magnesium deficiency. In conclusion, prolonged omeprazole treatment-induced small intestinal inflammation and villous atrophy, which led to decrease small intestinal magnesium absorption in the condition of proton pump inhibitor-induced hypomagnesemia. Keywords Hypomagnesemia · Inflammation · Proton pump inhibitors · Small intestine · Ultrastructure Abbreviations FBG Fast blood glucose IELs Intraepithelial lymphocytes M-to-S Mucosa-to-serosa PPIs Proton pump inhibitors PPIH PPI-induced hypomagnesemia TEER Trans-epithelial electrical resistance TJ Tight junction
* Narongrit Thongon [email protected] 1
Division of Anatomy, Department of Biomedical Sciences, Faculty of Allied Health Sciences, Burapha University, 169 Long‑Hard Bangsaen Rd., Saensook, Muang, Chon Buri 20131, Thailand
Division of Physiology, Department of Biomedical Sciences, Faculty of Allied Health Sciences, Burapha University, Chon Buri, Thailand
2
Introduction Proton pump inhibitors (PPIs) are common and effective medication to treat acid-peptic diseases. PPIs irreversibly bind to H+–K+ ATPase pump on the luminal surface of the parietal cell that leads to a suppression of gastric acid secretion. Adverse effects of prolonged PPIs administration are gastric mucosal atrophy, enlargement of the parietal and enterochromaffin-like cells, and decrease the number of gastric chief cells (Masaoka et al. 2008; Tanaka et al. 2019). How