Effect of long‐term administration of rebamipide on Helicobacter pylori infection in mice

Abstract

SUMMARYBackground: It has been suggested that chronic, persistent, uncontrolled inflammations in the stomach could provide the basic step for the beginning of carcinogenesis. One of the potential clinical applications of rebamipide is the inhibition of the immunoinflammatory response in gastric mucosa imposed by Helicobacter pylori. Aim: To determine the implications of long-term rebamipide treatment in H. pylori infection, we studied the underlying moleculo-pathological changes in gastric lesions in mice infected with H. pylori (SS1 strain), following this treatment. Methods: C57BL/6 mice were sacrificed 24 and 50 weeks after H. pylori infection, respectively. Colonization rates of H. pylori, degree of gastric inflammation and other pathological changes including atrophic gastritis and metaplasia, serum levels of IL-1b, TNF-a, IFN-c and IL-10, mRNA transcripts of various mouse cytokines and chemokines, and NF-jB binding activities, and finally the presence of gastric adenocarcinoma were compared between an H. pylori infected group

Effect of Rebamipide on the Colonic Barrier in Interleukin-10-Deficient Mice

“…The lack of effect of rebamipide on the Tcell stimulation markers, CD44 and CD62L, suggests that these markers are less sensitive parameters of T-cell stimulation than cytokine secretion, at least in our model. The immuno-stimulatory properties of rebamipide observed in this study are in contrast to the previous studies where an inhibitory effect was observed on immune response, both in vitro [23][24][25][26][27], and in vivo [9,[28][29][30]. This apparent contradiction may be explained by differences in the models used.…”

Inhibitory Activities and Attenuated Expressions of 5-LOX with Red Ginseng in Helicobacter pylori-Infected Gastric Epithelial Cells

“…According to Shimakura and Boland [34], under basal condition, gastric epithelial cell line, AGS-the same cell line used in the current experiment-produce LTD 4 as its principal eicosanoid metabolite followed by 6-keto-PGE 1 , LTC 4 , LTB 4 , 12-HETE, TXB 2 , PGF 2α , PGE 2 , 12-HETE, 15-HETE, and PGD 2 , but after stimulation with calcium ionophore, the principal eicosanoid metabolites become 12-HETE, followed by LTB 4 , LTC 4 , PGF 2α , PGE 2 , 6-keto PGF 1α , TXB 2 , LTD 4 , 15-HETE, and PGD 2 , suggesting that 5-LOX might be more active than COX in gastric epithelial cells. Their ability to metabolize AA differed according to cell context and each cell type may have a unique ability to produce PGs, HETEs, LTs, and other related eicosanoids.…”

“…Helicobacter pylori infection has been known to be associated with several pathologic alterations in stomach, including chronic gastritis, gastroduodenal ulcer, mucosa-associated lymphoid tissue lymphoma, and gastric adenocarcinoma [1][2][3][4], all of which were pathophysiologically based on chronic persistent gastric inflammations and crossroad between inflammation and carcinogenesis [5]. It has been shown that colonization of H pylori in the gastric mucosa induces a dramatic change in gastric mucosal phospholipid composition and elevates the metabolites of various eicosanoids from epithelial membrane phospholipid, which has been related to inflammatory host responses in infected gastric environment [5,6].…”

Clinical significance of expression of apoptotic signal proteins in gastric carcinoma tissue

“…Apoptotic abnormality is considered as an important mechanism underlying the development of gastric carcinoma [18,19] and even more crucial than the reproduction of cells of out control [20,21] . The expression of apoptotic signal proteins play different roles in the death of gastric cancer cells.…”