Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies of hepatocyte growth factor (HGF) in the stomach are briefly reviewed. Exogenous HGF has a strong effect on proliferation and migration of gastric epithelial cells. These effects of HGF are mediated by the specific receptor c-MET. Our previous immunohistochemical study revealed that the main source of endogenous HGF in human gastric ulcer is gastric fibroblasts. These findings suggest that HGF may play an important role in the repair of gastric ulcers through a paracrine mechanism. Therefore, regulation of HGF expression by gastric fibroblasts may be important. We have demonstrated that prostaglandins (PGs) E1 and E2 strongly stimulate HGF expression by gastric fibroblasts, indicating that the clinical efficacy of PGs is mediated by HGF, PGE1 actually facilitates restitution in an in vitro gastric mucosal model consisting of gastric epithelial cells and fibroblasts, which was completely inhibited by anti-HGF antibody. In this study we investigated the effect of an anti-ulcer drug, sofalcone, on PGE2 release and HGF expression by human gastric fibroblasts in primary culture. Sofalcone induced PGE2 release by human gastric fibroblasts in a dose-dependent manner. It also stimulated HGF expression by gastric fibroblasts, indicating that PGs induced by sofalcone increased HGF expression. These findings suggest that clinical efficacy of PGs and sofalcone might be mediated, at least in part, by HGF.
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PMID:Effect of sofalcone on the expression of hepatocyte growth factor (HGF) and a brief review of HGF in the stomach. 947 23

H. pylori and nonsteroidal antiinflammatory drugs (NSAIDs) are important factors in the recurrence of peptic ulcer diseases. However, H. pylori-negative recurring ulcers can also be found in nonusers of NSAIDs. The aim of this paper is to review recent data pertaining to mechanisms of ulcer recurrence. Prostaglandin E2 generation is impaired in the tissues of the ulcer scar site and prostaglandin depletion induced by administration of indomethacin during the healing of experimental gastric ulcer predisposes to future ulcer recurrence. Therefore, the prostaglandin deficiency may impair the quality of ulcer healing and thus increase the likelihood of future ulcer recurrence. Persistent infiltration of polymorphonuclear cells is the most prominent finding in the gastric ulcer scar in rats treated with indomethacin. Concomitant administration of prostaglandin E1-analog with indomethacin attenuates inflammatory infiltration and reduces future ulcer recurrence. Therefore, the inflammatory responses at the ulcer scar site may be a key to the quality of ulcer healing. Recent clinical findings suggest a close relationship between the quality of ulcer healing, infiltration of neutrophils and mononuclear cells, and future ulcer recurrence. Gastroprotective drugs such as prostaglandin analogs and prostaglandin inducers improve the quality of ulcer healing and reduce future recurrence. Production of inflammatory cytokines is stimulated by ulcerogenic factors such as NSAIDs, stress, and H. pylori infection. Inflammatory cytokines such as interleukin-1beta and tumor necrosis factor-alpha cause recurrence of healed ulcer. Synthetic prostaglandin E2 inhibits recurrence as well as the production of the cytokines.
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PMID:Ulcer recurrence: cytokines and inflammatory response-dependent process. 975 28

In the MUSE classification of gastroesophageal reflux disease (GERD), esophagitis is assessed by the presence of metaplasia, ulcer, stricture, or erosion, each being graded as absent, mild or severe. Daily reflux symptoms affect about 4 to 7 percent of the population; erosive esophagitis occurs in about 2 percent; the prevalence rate of Barrett's metaplasia is 0.4 percent; and esophageal adenocarcinoma leads to two deaths per million living population. In persons with GERD symptoms, about 20 percent are found to have erosive esophagitis, while ulcers or strictures are found in less than 5 percent of all patients with erosive esophagitis. No clear-cut temporal progression exists between successive grades of disease severity, as the most severe grade of GERD is reached at the onset of the disease. Mild forms of GERD tend to be more common in women than men, while severe GERD characterized by erosive esophagitis, esophageal ulcer, stricture or Barrett's metaplasia are far more common in men than women. All forms of GERD affect Caucasians more often than African Americans or Native Americans. The prevalence of GERD is high among developed countries in North America and Europe and relatively low in developing countries in Africa and Asia. During the past three decades, hospital discharges and mortality rates of gastric cancer, gastric ulcer and duodenal ulcer have declined, while those of esophageal adenocarcinoma and GERD have markedly risen. These opposing time trends suggest that corpus gastritis secondary to Helicobacter pylori infection protects against GERD. This hypothesis is consistent with the geographic and ethnic distributions of GERD. Case-control studies also indicate that cases with erosive esophagitis are less likely to harbor active or chronic corpus gastritis than controls without esophagitis.
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PMID:Clinical epidemiology and natural history of gastroesophageal reflux disease. 1078 May 69

We examined the involvement of cyclooxygenase (COX)-1 as well as COX-2 in the healing of gastric ulcers and investigated which prostaglandin (PG) EP receptor subtype is responsible for the healing-promoting action of PGE2. Male SD rats and C57BL/6 mice, including wild-type, COX-1(-/-), and COX-2(-/-), were used. Gastric ulcers were produced by thermocauterization under ether anesthesia. Gastric ulcer healing was significantly delayed in both rats and mice by indomethacin and rofecoxib but not SC-560 given for 14 days after ulceration. The impaired healing was also observed in COX-2(-/-) but not COX-1(-/-) mice. Mucosal PGE2 content increased after ulceration, and this response was significantly suppressed by indomethacin and rofecoxib but not SC-560. The delayed healing in mice caused by indomethacin was significantly reversed by the coadministration of 11-deoxy-PGE1 (EP3/EP4 agonist) but not other prostanoids, including the EP1, EP2, and EP3 agonists. By contrast, CJ-42794 (selective EP(4) antagonist) significantly delayed the ulcer healing in rats and mice. VEGF expression and angiogenesis were both upregulated in the ulcerated mucosa, and these responses were suppressed by indomethacin, rofocoxib, and CJ-42794. The expression of VEGF in primary rat gastric fibroblasts was increased by PGE2 or AE1-329 (EP4 agonist), and these responses were both attenuated by coadministration of CJ-42794. These results confirmed the importance of COX-2/PGE2 in the healing mechanism of gastric ulcers and further suggested that the healing-promoting action of PGE2 is mediated by the activation of EP4 receptors and is associated with VEGF expression.
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PMID:Cyclooxygenase-2/prostaglandin E2 accelerates the healing of gastric ulcers via EP4 receptors. 1767 47


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