Disease relevance of D01121

• Rebamipide, a novel antiulcer agent, attenuates Helicobacter pylori induced gastric mucosal cell injury associated with neutrophil derived oxidants [1].
• Rebamipide, a novel antiulcer agent, has been reported either to prevent various acute experimental gastric mucosal lesions or to accelerate the healing of chronic gastric ulcers [2].
• Intraperitoneal administration of rebamipide at 60 mg/kg body weight reduced gastric mucosal hemorrhagic lesions and lipid peroxidation, which was proportional to the inhibitory effect of rebamipide on alcohol-induced xanthine oxidase-type conversion and enzyme activity [3].
• Clinically, it is suggested that rebamipide has the potential to prevent gastric carcinogenesis by improvement of histological gastritis [4].
• Total RNA was extracted from MKN45 cells, a human gastric cancer cell line, following HPE-stimulation with and without rebamipide for 3 h, and differences in gene expression profiles were observed using GeneChip and Human 6800 probe array [5].

Psychiatry related information on D01121

• These results suggest that rebamipide may strengthen the host defense mechanisms related to carcinogenesis in the digestive tract [6].
• In rats treated with rebamipide, clinical (body weight loss, bloody diarrhea, reduced physical activity, severe anemia, shortened colonic length, and perianal injury) and histopathological (pathological lesion score) findings of DSS colitis were significantly less than in rats with DSS colitis not treated with rebamipide [7].

High impact information on D01121

• The effect of rebamipide, a novel antiulcer compound, on Helicobacter pylori activated neutrophil dependent in vitro gastric epithelial cell injury was investigated [1].
• Hydroxyl radical scavenging by rebamipide and related compounds: electron paramagnetic resonance study [8].
• The aim of this work was to study the capacity of Helicobacter infection to inhibit the development of oral tolerance or to promote allergic sensitization and the capacity of a gastro-protective agent, rebamipide, to interfere with these processes in mice [9].
• H. felis infection led to the inhibition of oral tolerance to OVA, but rebamipide prevented this inhibitive effect of H. felis [9].
• Additionally, the capacity of rebamipide to interfere with antigen presentation and T-cell activation in vitro, as well as absorption of rebamipide across the epithelial monolayer, was tested [9].

Chemical compound and disease context of D01121

• Comparison of the effects of rebamipide with those of cimetidine on chronic gastritis associated with Helicobacter pylori in Mongolian gerbils [10].
• Chronic administration of rebamipide (100 mg/kg/day, p.o., for 3 wk) to rats, in which diabetes was previously induced by the i.v. injection of streptozotocin 50 mg/kg, reversed hyperglycemia, which would contribute to prevent the increases in urinary excretion rates of albumin and lipid peroxides observed in this experimental model [11].
• Bile flow and cholate output were markedly decreased by ischemia/reperfusion and free radical scavengers, especially rebamipide, restored their secretion [12].
• Aminopyrine N-demethylase activity was decreased and aniline p-hydroxylase was increased by ischemia/reperfusion, which were prevented by alpha-tocopherol and allopurinol, but not by rebamipide [12].
• The aim of this study was to examine the efficacy of rebamipide on acetic acid-induced colitis in rats [13].

Biological context of D01121

• On the other hand, the viabilities of H. pylori, MKN-28 cells, and MKN-45 cells were not affected by rebamipide [14].
• CONCLUSIONS: These findings suggest that rebamipide could inhibit inflammatory reactions and tumour progression by modifying H. pylori infection-induced gene expression in gastric epithelial cells [5].
• Rebamipide, however, did not affect neutrophil apoptosis and caspase-3 activity [15].
• Using the unfixed cryostat sections, aqueous solution of 3H-rebamipide was applied and the localization of the binding sites of rebamipide was investigated by autoradiography [16].
• In an in vitro study, rebamipide inhibited N-formyl-met-leu-phe-induced chemotaxis of neutrophils and production of superoxide anion from opsonized zymosan-stimulated neutrophils [17].

Anatomical context of D01121

• This change was significantly attenuated by rebamipide at a concentration less than 1 mM, showing that rebamipide may inhibit oxidant production from H pylori elicited neutrophils [1].
• Our studies suggest that rebamipide inhibits the adhesion of H. pylori to gastric epithelial cells [14].
• Rebamipide has many biological activities for gastric mucosa such as increasing the blood flow and biosynthesis prostaglandins and the decrease of oxygen radicals [4].
• Taken together, this study demonstrates that rebamipide inhibits neutrophil adhesion to HUVECs by a mechanism involving inhibition of transcription-dependent surface expression of E-selectin and P-selectin in H/R-stimulated endothelial cells [18].
• These properties of rebamipide could explain its anti-inflammatory activity with respect to the digestive mucosa and could provide protection against allergic sensitization to foreign antigens in susceptible individuals [19].

Associations of D01121 with other chemical compounds

• We compared these effects of rebamipide with those of cimetidine in Mongolian gerbils infected with H. pylori [10].
• Combination of autoradiography and immunohistochemistry has revealed that iNOS-immunoreactive cells had the strong binding of rebamipide in the acetic acid-treated group [16].
• Rebamipide suppressed PGE2 secretion from neutrophils dose-dependently [15].
• These results provide evidence that the competitive inhibitory action of rebamipide on the fMLP-receptor plays a main role in its inhibitory action on fMLP-induced O2 production [20].
• In this study, we evaluated the effect of rebamipide, an antigastritis and antiulcer agent, on H. pylori-dependent ceramide production and subsequent interleukin-8 expression in Kato III cells [21].

Gene context of D01121

• Rebamipide pretreatment reduced both COX-2 expression and IR injury [22].
• It is therefore suggested that the hydroxylation of rebamipide only involves CYP3A4 [23].
• The PCNA-labelled epithelial cells in the rebamipide group were also greater than in the control group on days 10, 30, 90 and 120 (P < 0.05, each) [24].
• Rebamipide suppressed the production of IL-8, IL-10, TNF-alpha, and IL-1beta induced by H. pylori in a dose-dependent manner [25].
• SC-560, a selective COX-1 inhibitor; NS-398, a selective COX-2 inhibitor; or rebamipide, a mucoprotective agent, was administered to mice 60 min before ischemia [22].

Analytical, diagnostic and therapeutic context of D01121

• We studied the scavenging activity of rebamipide, a novel antipeptic ulcer agent, and seven related compounds against hydroxyl radicals using the electron paramagnetic resonance (EPR) spin trapping technique [8].
• Western blot analysis showed that induction of heat-shock protein (HSP70) was significantly increased following rebamipide administration in a dose-dependent manner [2].
• We evaluated the effect of rebamipide on H. pylori adhesion to MKN-28 and MKN-45 cells quantitatively using our previously established enzyme-linked immunosorbent assay [14].
• We investigated the effect of rebamipide on rat gastric mucosa damaged by exposure to 30 min of ischemia and 60 min of reperfusion (I/R) with continuous intragastric instillation of 0.1 N HCl (1 ml/100 g body weight) into the stomach [17].
• Double-blind placebo-controlled multicentre studies of rebamipide, a gastroprotective drug, in the treatment of functional dyspepsia with or without Helicobacter pylori infection [26].

References