Injury to the Gastric Mucosa and Cellular Dynamics in a Rat Model of Duodenogastric Reflux: The Possible Significance of Gastrin Induction and a Heat Shock Protein

Abstract

Injury to the gastric mucosa caused by duodenogastric reflux (DGR) is often encountered after gastrectomy or truncal vagotomy (V) with pyloroplasty. This study was designed to investigate the histological features of the gastric mucosa under such conditions. A rat model of DGR and DGR+V was established and the thickness of the oxyntic mucosa was measured. Cellular dynamics in the presence of injury to the gastric mucosa caused by DGR were investigated by the immunohistochemical staining of bromodeoxyuridine (BrdU) and heat shock protein 70 (HSP70). The relationship between persistent hypergastrinemia and mucosal injury was also studied. Duodenogastric reflux activated the intracellular induction of HSP70 in our rat model of DGR. Hypergastrinemia was noted in the V group. Compared with values from the DGR group, the numbers of BrdU-labeled cells increased, the glandular proliferation zone expanded, and the thickness of the oxyntic mucosa was significantly higher in the DGR+V group. Compared with the DGR group, there was greater induction of HSP in the DGR+V group during the acute stage. This finding suggests that denervation of the gastric mucosa and hypergastrinemia after vagotomy may be associated with the expression of HSP.

Protective effects of heat shock protein70 induced by geranylgeranylacetone in atrophic gastritis in rats

“…Atrophic gastritis results from the long-term gastric damages that impair the adaptive cytoprotection of gastric mucosa. In recent years, the mechanism that protects the gastric mucosa against intrinsic and extrinsic stimuli and maintains the proper structure and function of the gastric mucosa has attracted considerable attention [5] . Heat shock protein (HSP) 70, one of the major molecular chaperons, can adapt cells to cope with various stresses in gastric mucosa [6] and accelerate the cellular recovery from different stimuli by coping with unfolded or denatured proteins [7] .…”

Muscovite Reverses Gastric Gland Atrophy and Intestinal Metaplasia by Promoting Cell Proliferation in Rats with Atrophic Gastritis

“…In fact, except for the eradication of H. pylori , the regeneration of the gastric gland was considered a remarkable factor when referred to intervention of AG. In recent years, the mechanism that protects the gastric mucosa against intrinsic and extrinsic stimuli and maintains the proper structure and function of the gastric mucosa has attracted considerable attention [9]. The gastric mucosa continuously renews epithelial cells by maintaining the balance of cell proliferation and apoptosis.…”