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)

A study was made of the effect of copper laser therapy on the content of PGE and PGF2 alpha and on the adenylate cyclase system (cAMP, cGMP and adenylate cyclase content) in patients with gastric ulcer. Seventy patients with indolent (from 3 months to 2 years) gastric ulcers were examined. The patients were assigned into 2 groups: group I received drug therapy combined with the influence of laser on copper vapours on the ulcerous surface (a single radiation dose 10 to 15 J). As compared to group I, the patients of group II manifested a considerable rise of the content of cAMP and prostaglandins, as well as adenylate cyclase activation in the gastric mucosa. Nonspecific biostimulating action of laser radiation exercised via the influence on the dysregenerative processes in the epitheliocytes of long nonhealing ulcer edges is under discussion.
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PMID:[The effect of laser therapy on the mechanisms for generating healing in long-term nonhealing stomach ulcers]. 233 23

Gastric ulcer (GU) and duodenal ulcer (DU) occur as a result of the imbalance between aggressive and defensive factors affecting the gastroduodenal mucosa. Prostaglandins (PG) of E and I series are generated throughout the gastrointestinal tract, particularly in the gastric and duodenal mucosa, and are released into the gut lumen upon vagal and hormonal stimulation. Endogenous PGs may be involved in the maintenance of mucosal integrity, control of mucosal blood flow and protection against potentially noxious agents. Gastric mucosa of ulcer patients tends to generate smaller amounts of PGs of E and I series and exhibits a reduced ratio of PG to thromboxane generation, which suggests that the deficiency of protective PG may play a role in the pathogenesis of peptic ulcer. Suppression of mucosal generation of PGs by non-steroidal anti-inflammatory compounds causes mucosal damage and increases the risk of the formation or exacerbation of peptic ulcer. Exogenous PGE and its stable analogs have been tested successfully in the treatment of GU and DU and the results so far obtained indicate that these agents significantly increase the ulcer healing rate. Certain anti-ulcer drugs such as carbenoxolone, sucralfate, colloidal bismuth and cimetidine appear to exert their beneficial effects on ulcer healing by mediating the release of endogenous PGs.
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PMID:Prostaglandins in pathophysiology of peptic ulcer disease. 386 51

Prostaglandin E was measured by radioimmunoassay in endoscopic biopsy specimens obtained from 7 normal healthy volunteers, 28 patients with a benign gastric ulcer, and 10 with a malignant gastric ulcer. Biopsy specimens were taken from the antral and body mucosa and from the ulcer edge in patients. The median value in normal antrum specimens was 5.15 (4.44-8.40) ng PGE/mg protein which was more than the body with 3.50 (1.86-9.28), p less than 0.05. In the 28 patients with benign gastric ulcer the ulcer edge contained 2.33 (0.48-7.67) ng PGE/mg protein which was more than the antrum with 1.06 (0.30-4.17) or the body with 0.97 (0.20-7.67), p less than 0.01 respectively. The antral and body levels in patients with gastric ulcers were lower than those found in the normal volunteers, p less than 0.01. There was no difference between the levels found in patients with malignant as opposed to benign gastric ulcer. In patients with gastric ulcer lower levels of PGE were found in body mucosa with atrophic gastritis 0.83 (0.53-2.66) ng PGE/mg protein as compared with histologically normal body mucosa 2.55 (0.63-7.67), p less than 0.05. These results suggest that mucosal PGE levels are reduced in patients with gastric ulcer disease and that this may be due to the presence of atrophic gastritis.
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PMID:Gastric mucosal prostaglandin E levels in patients with gastric ulcer disease and carcinoma. 705 27

Nonsteroidal anti-inflammatory drugs (NSAIDs) are most frequently used for the treatment of rheumatic disease due to their anti-inflammatory and analgesic properties. All NSAIDs have the potential to cause damage to the gastrointestinal (GI) tract and have been associated with the induction of peptic ulcers and massive life-threatening bleeding. The therapeutic approaches for the treatment and prevention of NSAID-induced ulcers is critically reviewed using data derived from carefully controlled, world-wide clinical studies with anti-ulcer drugs. Histamine (H2) antagonists, omeprazole, sucralfate and E-prostaglandin (PGE) analogs are effective for the treatment of NSAID-induced gastric and duodenal ulcers, if NSAIDs are discontinued. However, if NSAIDs are continued while GI damage is present, the PGE analogs misoprostol, arbaprostil and enprostil have shown efficacy in healing NSAID-induced ulcers. Furthermore, one limited clinical study demonstrated that omeprazole has efficacy in healing NSAID-associated ulcers. Neither H2 antagonists, sucralfate and sulglycotide (a cytoprotective drug) have shown efficacy in preventing NSAID-induced gastric ulcers. However H2 antagonists have shown efficacy in preventing NSAID-induced duodenal ulcers. In contrast, only misoprostol prevents the development of NSAID-induced gastric and duodenal ulcers. Such pharmacological observations suggest that the pathophysiologic mechanisms for the induction of NSAID-induced gastric ulcer are distinctly different from those of NSAID-induced duodenal ulcers. Mild diarrhea and GI intolerance were the predominant adverse reactions experienced by patients receiving synthetic PGEs, particularly enprostil and arbaprostil. From the published data, we conclude that misoprostol is the only anti-ulcer drug proven to be well tolerated and effective for the treatment and prevention of NSAID-induced gastric and duodenal ulcers in patients receiving chronic NSAIDs therapy.
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PMID:Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs: an update. 759 35

Measurements of serum IL-1 levels and PGE-2 content in biopsies from gastric mucosa at ulcer margins were made in 30 patients with gastric ulcer running differently. The highest IL-1 production and low PGE-2 levels were typical for healing ulcer. Cicatrization was accompanied with normalization of IL-1 and PGE-2 values. Gastric ulcer with a severe course exhibited inhibited IL-1 synthesis and decreased production of PGE-2.
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PMID:[Prostaglandins E concentration in gastric mucosa and synthesis of interleukin-1 (IL-1) in different clinical variants of gastric ulcer]. 899 50

It has been assumed that cyclooxygenase-2 (COX-2) is solely responsible for inflammatory processes. Recently, this view has been challenged because COX-2-selective agents caused a delay of gastric ulcer healing and exacerbation of inflammation in rats. To further characterize organ-specific toxic effects of selective and nonselective COX inhibitors, we assessed the eicosanoid release from different rat organs ex vivo after oral administration of the COX-2-selective inhibitor NS-398 and the unselective COX inhibitors diclofenac, meloxicam, and ketorolac. Prostanoid and leukotriene release from tissue fragments of the stomach, kidney, lung, and brain were determined after ex vivo incubation of tissue fragments in Tyrode's solution for 10 min at 37 degrees C. Ketorolac (0.1, 0.3, and 0.9 mg/kg) inhibited prostanoid release from all organs most potently and led to a significant increase of leukotriene release from the lung. Effects of diclofenac and meloxicam (1, 3, and 9 mg/kg each) were similar for all organs tested. At 9 mg/kg, 6keto-prostaglandin F (PGF)(1alpha) release from gastric mucosa was reduced by 79.1 +/- 11.4 and 87.6 +/- 7.7% and PGE(2) release from rat kidney was inhibited by 60.4 +/- 6.8 and 78.6 +/- 16.6% by diclofenac and meloxicam, respectively. NS-398 did not reduce prostanoid release from the lung. Consistent with the reported constitutive expression of COX-2, prostanoid release from kidney and brain was reduced by 20 to 30%. The release of 6keto-PGF(1alpha) from gastric mucosa was reduced by 34.7 +/- 22.2% at 3 mg/kg and by 86.9 +/- 12.7% at 9 mg/kg. At these doses, NS-398 has been previously shown to be COX-2 selective. Because PGF(1alpha) is the stable breakdown product of PGI(2), these results suggest that COX-2 contributes to PGI(2) synthesis in the rat stomach.
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PMID:Effects of selective and unselective cyclooxygenase inhibitors on prostanoid release from various rat organs. 1068 36

The effect of hypotonic medium (Distilled water: DW) and hypertonic saline (HS: 5% NaCl) compared to control normal saline (NS) was studied on gastric ulcer induced by aspirin, 6 h cold restraint stress, ethanol, and pylorus ligation in rats. DW did not afford any protection while HS showed significant ulcer protective effects in all gastric ulcer models studied. The cytoprotective effect of HS seemed to be not only due to its effect on gastric acid secretion but also its effect on mucosal defensive factors like enhanced mucin secretion and decreased cell shedding. As determined by radioimmunoassay, DW did not produce any change in the accumulation of PGE and PGI2, while HS increased them significantly in the human gastric mucosal incubates compared to NS. However, in the incubates of human colonic mucosa, both DW and HS showed a significant increase in PGE with a tendency to increase in PGI2 accumulation.
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PMID:Effect of mild irritant on gastric mucosal offensive and defensive factors. 1084 33

We investigated the role of nuclear factor-kappaB (NF-kappaB) in gastric ulcer healing in rats. NF-kappaB was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer healing. NF-kappaB activation was observed in fibroblasts, monocytes/macrophages, and neutrophils. Treatment of gastric fibroblasts, isolated from the ulcer base, with interleukin-1beta activated NF-kappaB and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-kappaB action resulted in suppression of both their mRNA expression and increases in PGE(2) and CINC-1 levels induced by interleukin-1beta. Persistent prevention of NF-kappaB activation caused an impairment of ulcer healing in rats. Gene expression of interleukin-1beta, CINC-1, cyclooxygenase-2, and inducible nitric oxide synthase in ulcerated tissue had been inhibited before the delay in ulcer healing became manifest. The increased levels of cyclooxygenase-2 protein and PGE(2) production were also reduced. These results demonstrate that NF-kappaB, activated in ulcerated tissue, might upregulate the expression of healing-promoting factors responsible for gastric ulcer healing in rats.
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PMID:Role of nuclear factor-kappaB in gastric ulcer healing in rats. 1135 24

Selective cyclooxygenase-2 (COX-2) inhibitors have been shown to produce fewer gastrointestinal adverse reactions when compared with conventional nonselective nonsteroidal anti-inflammatory drugs and they suppress angiogenesis in tumors. The purpose of the present study was to investigate the effects of highly selective COX-2 inhibitor on angiogenesis and protein expression of angiogenic factor during gastric ulcer healing. Gastric ulcers were induced in male Sprague-Dawley rats by a luminal application of acetic acid solution. Rofecoxib, a selective COX-2 inhibitor, was administered at a dose of 10 mg/kg/day by gastric intubation for 14 successive days. The ulcer size was measured at different time intervals after ulcer induction. The microvessels that were immunohistologically positive for von Willebrand factor within the ulcer bed were counted. The protein levels of basic fibroblast growth factor (bFGF) and concentration of prostaglandin E(2) (PGE(2)) in the ulcer tissues were analyzed with Western blotting and immunoassay methods, respectively. The results demonstrated that rofecoxib treatment significantly increased the ulcer size at days 6, 10, and 15. It decreased the number of microvessels, bFGF protein expression, and PGE(2) level in the ulcer base at day 6. The findings that highly selective COX-2 inhibitor delayed ulcer healing in rats and impaired angiogenesis in the ulcer base raise cautions regarding the use of COX-2 inhibitors in patients with gastric ulcers.
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PMID:Antiangiogenic effect of a highly selective cyclooxygenase-2 inhibitor on gastric ulcer healing in rats. 1221 40

Bacopa monniera is an Indian tratidional medicine widely used to improve intellectual functions. Earlier, we had reported the prophylactic and curative effects of standardized extract of Bacopa monniera (BME) in various gastric ulcer models. The effect was due to augmentation of the defensive mucosal factors like increase in mucin secretion, life span of mucosal cells and gastric antioxidant effect rather than on the offensive acid-pepsin secretion. The present study includes evaluation of standardized BME (bacoside A content--35.5 +/- 0.9) on other contributing factors towards ulcerogenesis. BME in the dose of 1000 microg/ml showed anti-Helicobacter pylori activity in vitrol and in the dose of 10 microg/ml increased in vitro of prostanoids (PGE and PGI2) in human colonic mucosal incubates. It may be concluded that these factors may contribute to antiulcerogenic activity of BME.
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PMID:In vitro evaluation of Bacopa monniera on anti-Helicobacter pylori activity and accumulation of prostaglandins. 1367 38


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