Histopathology and ultrastructural alterations in gastric mucus-secreting cells in diabetic model rats

Abstract

Diabetes mellitus (DM) can cause gastric ulcers (GU), duodenal ulcers (DU), and gastroesophageal reflux disease (GERD). Mucus-secreting cells secrete mucus, which aids in the neutralization of HCl and inhibits bacteria. DM can alter mucus-secreting cells. Due to a lack of mucosal defense, external stimuli such as bacteria or ethanol can lead to the development of GU, DU, and GERD. This research study used a STZ-induced diabetic rat model to examine the short- and long-term histopathology and ultrastructural alterations in mucus-secreting cells in the cardia, body, and pyloric regions of the stomach. Quantitative analysis was also employed in this study to examine the distribution of mucin granules across all three locations. Twenty-four male adult Sprague-Dawley rats were utilized. Rats were divided into the control (n = 12) and DM (n = 12) groups. Each was separated into short-term (4 weeks) and long-term (24 weeks) rats. For DM induction, streptozotocin (STZ) can selectively destroy the beta cells of the pancreas. The DM was injected with STZ in citrate buffer at 60 mg/kg body weight. The control group was injected with citrate buffer. Histopathology was examined by Alcian blue-Periodic Acid Schiff staining under a light microscope. Image analysis was applied to quantify mucin accumulation. The ultrastructure was explored using transmission electron microscopy. In short-term and long-term DM, there was superficial erosion of the gastric epithelium and a significant decrease in the percentage of mucin granule accumulations in both surface mucous cells (SMCs) and mucous neck cells (MNCs). In short-term DM, SMCs were degenerated with vacuolation, disrupted cristae of mitochondria, and dilated rough endoplasmic reticulum (rER). MNCs were swollen with destroyed organelles. In long-term DM, degenerative nuclei and electron-lucent regions with unidentified structures of SMCs were observed. Nuclear chromatin condensation and the disappearance of mucin granules were present in MNCs. In conclusion, under both LM and TEM, STZ-induced diabetic rats demonstrated both short- and longterm damage to the gastric mucosa and gastric gland structures.