Chronic (Nonerosive) Gastritis: Pathogenesis and Management

Talley, Nicholas J.

doi:10.1159/000171207

Cited by 13 publications

(1 citation statement)

References 51 publications

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“…A number of studies have shown that reactive oxygen species (ROS) are involved in the pathogenesis of a variety of gastroduodenal diseases, such as those induced by ischaemia/reperfusion, 10 ethanol (EtOH) 11 , 12 or nonsteroidal anti‐inflammatory drugs (NSAIDs) 13 , . 14 Helicobacter pylori causes type B chronic gastritis, 15 which becomes a long‐standing and life‐long gastritis if it is not eradicated 16 . In gastric mucosa with H. pylori infection, active inflammation with infiltration of neutrophils in the acute stage of the infection and of macrophages/monocytes, lymphocytes and plasma cells in the chronic stages are seen in the lamina propria of the stomach 17 , .…”

Section: Introductionmentioning

confidence: 99%

Polaprezinc protects gastric mucosal cells from noxious agents through antioxidant properties in vitro

Hiraishi

Sasai

Oinuma

et al. 1999

Aliment Pharmacol Ther

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Background: Polaprezinc has been shown to exert an anti‐oxidant property in a tube experiment, protect gastric mucosa from experimental ulcerations in vivo, and accelerate the healing of gastric ulcer in humans. Aim: To examine a possible protective effect of polaprezinc on oxidant‐mediated injury in primary monolayer cultures of rat gastric fundic mucosa. Methods: Cytotoxicity was quantified by measuring 51Cr release. Whether or not polaprezinc exerts an antioxidant property was investigated by determining the effect of this agent on hydrogen peroxide (H2O2)‐induced injury. The effects of polaprezinc on superoxide (O2–·) generation as well as on ethanol (EtOH)‐induced injury were also examined. Generation of O2–· was assessed by the reduction in cytochrome c. Results: H2O2 caused a time‐ and dose‐dependent increase in 51Cr release. The dose‐response curve of 51Cr release by H2O2 shifted to the right in the presence of polaprezinc. Polaprezinc, at submillimolar concentrations, prevented H2O2‐induced 51Cr release. EtOH also caused a dose‐dependent increase in 51Cr release, which was prevented by the addition of polaprezinc. The incubation of cells with EtOH caused an increase in cytochrome c reduction, as the concentrations of EtOH increased. Polaprezinc inhibited EtOH‐induced cytochrome c reduction. Protection by polaprezinc was microscopically associated with the prevention of monolayer disruption. Conclusions: Polaprezinc is antioxidative and directly protects gastric mucosal cells from noxious agents through its antioxidant properties in vitro. This finding may provide the theoretical basis for the usage of an antiulcer drug with antioxidant properties for the treatment of gastric inflammation, such as that induced by ethanol.

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