[Progress in study for mechanism of gastric mucosal injury].
Inflammatory reactions mediated by leukocytes, cytokines, adhesion molecules, active oxygen species, nitric oxide(NO) or prostaglandins have been implicated in the pathogenesis of gastric mucosal injury induced by Helicobacter pylori(H. pylori) or nonsteroidal anti-inflammatory drugs(NSAID). The molecular mechanism of gastric mucosal injury has been investigated in view of cell proliferation, apoptosis or necrosis. Eradication therapy of H. pylori, Cox2 inhibitors or NO-releasing NSAID may become new strategy for protection against gastric mucosal injury.
Yoshida
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First Department of Internal Medicine, Kyoto Prefectural University of Medicine.
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D015815:Cell Adhesion Molecules / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D005753:Gastric Mucosa; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D007962:Leukocytes; D009569:Nitric Oxide / Q000502:physiology; D009853:Omeprazole / Q000627:therapeutic use; D011453:Prostaglandins / Q000502:physiology; D054328:Proton Pump Inhibitors; D017382:Reactive Oxygen Species; D013272:Stomach Diseases / Q000188:drug therapy / Q000209:etiology*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D015815:Cell Adhesion Molecules; D016207:Cytokines; D018836:Inflammation Mediators; D011453:Prostaglandins; D054328:Proton Pump Inhibitors; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D009853:Omeprazole