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)

Starting from the multiple role zinc holds in the enzymatic processes of the body and from some positive data concerning treatment with zinc sulphate in gastric ulcer, we have studied the effect of ZnSO4 on gastric acid secretion in duodenal ulcer patients, as well as that on purified and gastric mucosa carbonic anhydrase. Gastric secretory testing showed that zinc sulphate administered in doses of 60 ml/day (1% solution) for 10 days reduced basal acid secretion in duodenal ulcer patients by 57.7%. In vitro, concentrations of ZnSO4 ranging between 10(-6) and 10(-2)M, inhibit purified carbonic anhydrase activity in a dose-dependent manner, reaching maximum effect at 10(-2)M, when carbonic anhydrase activity dropped from 2060 +/- 65 IU to 660 +/- 85 IU. A similar dose-dependent inhibition was found with gastric mucosa carbonic anhydrase activity, where ZnSO4 at 10(-2)M reduces enzyme activity from its basal value of 1.58 +/- 0.36 EU/mg to 0.88 +/- 0.21 EU/mg. Besides this effect, zinc sulphate antagonized in vitro the activation of both purified and gastric mucosa carbonic anhydrase by histamine. In conclusion, the mechanism of antisecretory effect of ZnSO4 might well be the inhibition of the carbonic anhydrase in the gastric mucosa.
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PMID:Effect of ZnSO4 upon gastric acid secretion and carbonic anhydrase. 407 13

The effects of a new carbenoxolone analogue (BX24), zinc sulphate, and vitamin A on the healing of gastric ulcer have been assessed in a multifactorial clinical trial conducted in out-patients treated for four weeks.Forty-eight patients completed the trial. Three groups of eight patients were given respectively 300, 600, and 1 200 mg of BX24 daily and were compared with 24 patients who were given 300 mg of carbenoxolone sodium daily. The size of the ulcer niche was reduced on average by 14.6% in the eight patients given BX24 300 mg daily, by 47.6% in the patients given 600 mg daily, and by 51.0% in the patients given 1 200 mg daily. In the patients given carbenoxolone the size of the niche was reduced by 68.9%. These results were compared with those obtained previously with carbenoxolone and inert tablets and it was concluded that BX24 is without clinically useful effect in the doses used. Eleven of the 24 patients (46%) treated with carbenoxolone sodium developed side effects due to fluid retention and electrolyte disturbances. None of the patients given BX24 experienced such effects. In addition to carbenoxolone or BX24, 24 patients were given zinc sulphate, 660 mg daily, and in 24 patients these tablets were withheld. Among the patients given carbenoxolone the reduction in the size of the niche was much the same irrespective of whether or not the patients received zinc sulphate. Among the 12 patients given BX24 with zinc sulphate the ulcer healed completely in four and, on average, the size of the niche was reduced by 53.5%, compared with 21.9% in the 12 patients given BX24 alone. This difference is not statistically significant but the possibility of a beneficial effect from zinc is not excluded. No side effects attributable to zinc were observed.Twenty-four patients were also given vitamin A, 50 000 units daily, and in 24 patients the vitamin was withheld. No evidence was obtained to suggest that vitamin A had any beneficial effect on the healing of gastric ulcer.
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PMID:Clinical trial of a new carbenoxolone analogue (BX24), zinc sulphate, and vitamin A in the treatment of gastric ulcer. 455 8

Zinc is an important element in wound healing. Zinc compounds hasten the healing of gastric ulcers, by an unknown mechanism(s). We studied the effect of the induction of zinc deficiency on gastric ulcer healing. Rats were given a control or zinc-deficient diet for six weeks and then subjected to the induction of acetic acid-induced chronic gastric ulcers. Four days later, zinc-deficient rats were divided into two groups. In the first group, the zinc-deficient diet was continued. In the second group, the diet was changed to the control diet. Zinc-deficient rats had a mean serum zinc concentration approximately 70% of that in controls. Zinc deficiency did not affect the formation of gastric ulcers; however, it reduced cell proliferation by day 4 and delayed ulcer healing. Zinc supplementation brought zinc to control levels within a week, but failed to reverse the delay in ulcer healing. We conclude that zinc is crucial for healing of gastric ulcers, especially at the early stage.
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PMID:Zinc deficiency delays gastric ulcer healing in rats. 778 57

18 rats were randomly deivided into 3 groups: control grup, the group merely with experimental gastric ulcer and the group with experimental gastric ulcer after 3-week moxibustion. The results showed: (1) moxibustion could significantly reduce the ulcer area of the rats (P < 0.05); (2) compared with control group, the experimental gastric ulcer model rats had an increase in copper content and Cu/Zu ratio, the differences were statistically significant (P < 0.05, P < 0.01); (3) in contrast to the rats merely with experimental gastric ulcer, moxibustion-pretreated rats had a significant increase in Zinc content in serum (P < 0.01), but its copper content and Cu/Zn ratio in serum were significantly decreased (P < 0.05, P < 0.01). The results confirmed that moxibustion pretreatment at "Shen-Jue" could protect the gastric mucosa from strass-induced ulcer, having protective effect on gastric mucosa. The results also suggested that there was a disbalance in trace elements metabolism, but moxibustion could improve it. This was most likely to be one of the mechanisms of moxibustion protection on gastric mucosa.
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PMID:[The effect of moxibustion on gastric mucosa in rats and its relation to copper, zinc contents in serum]. 870 70

The fluorescence spectroscopy of porphyrin molecule in blood was determined with photoluminescence fluorescence spectroscope in 139 patients with gastric carcinoma, 76 with hepatic carcinoma, 110 with gastric ulcer and chronic gastritis, 168 with liver cirrhosis and 33 normals as controls. The results showed that the peaks of Zinc porphyrin and protoporphyrin in patients with cancer were significantly higher than those in patients with benign disease, the peak of protoporphyrin being two to three times higher in the former groups of patients than that in the latter (P < 0.01). Protoporphyrin could be used as a marker to screen and diagnose gastric and hepatic carcinoma.
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PMID:[Changes in hematoporphyrin in patients with gastric and hepatic carcinoma and their clinical significance]. 873 9

This study was undertaken in rats to ascertain the role of zinc as an antiulcerogenic agent employing its more bioavailable gluconate derivative. Pretreatment with zinc gluconate 10 mg/kg body wt orally for three consecutive days, protected against alcohol induced gastric epithelial damage and also significantly prevented non-steroidal anti-inflammatory drugs (NSAID) induced gastric ulcer in rats. The enhanced levels of mucus, and hexosamine and decreased acid output in the gastric secretion of zinc treated rats, increased the gastric mucosal barrier. Studies on the mechanism of action suggested the involvement of -SH groups in producing gastric antisecretory effect. Thus, zinc gluconate at > > 100 microM concentrations inhibited H(+)-ion transport which could be reversed by incorporating beta-mercaptoethanol in the secretory solution (luminal side). On the other hand, beta-mercaptoethanol added from the nutrient side showed no effect on the inhibition of H(+)-transport indicting that the implication of -SH groups may not be the sole factor. Zinc appeared to play a vital and multifaceted protective role in chemically induced gastric ulcer disorders.
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PMID:Protective effect of zinc gluconate on chemically induced gastric ulcer. 924 12

All cells, from bacterial to human, have a common, intricate response to stress that protects them from injury. Heat shock proteins (Hsps), also known as stress proteins and molecular chaperones, play a central role in protecting cellular homeostatic processes from environmental and physiologic insult by preserving the structure of normal proteins and repairing or removing damaged ones. An understanding of the interplay between Hsps and cell stress tolerance will provide new tools for treatment and drug design that maximise preservation or restoration of health. For example, the increased vulnerability of tissues to injury in some conditions, such as ageing, diabetes mellitus and menopause, or with the use of certain drugs,, such as some antihypertensive medications, is associated with an impaired Hsp response. Additionally, diseases that are associated with tissue oxidation, free radical formation, disorders of protein folding, or inflammation, may be improved therapeutically by elevated expression of Hsps. The accumulation of Hsps, whether induced physiologically, pharmacologically, genetically, or by direct administration of the proteins, is known to protect the organism from a great variety of pathological conditions, including myocardial infarction, stroke, sepsis, viral infection, trauma, neurodegenerative diseases, retinal damage, congestive heart failure, arthritis, sunburn, colitis, gastric ulcer, diabetic complications and transplanted organ failure. Conversely, lowering Hsps in cancer tissues can amplify the effectiveness of chemo- or radiotherapy. Treatments and agents that induce Hsps include hyperthermia, heavy metals (zinc and tin), salicylates, dexamethasone, cocaine, nicotine, alcohol, alpha-adrenergic agonists, PPAR-gamma agonists, bimoclomol, geldanamycin, geranylgeranylacetone and cyclopentenone prostanoids. Compounds that suppress Hsps include quercetin (a bioflavinoid), 15-deoxyspergualin (an immunosuppressive agent) and retinoic acid. Researchers who are cognisant of the Hsp-related effects of these and other agents will be able to use them to develop new therapeutic paradigms.
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PMID:Heat shock proteins: new keys to the development of cytoprotective therapies. 1599 80

Acute cold stress caused lesions of gastric mucosa as a result of its attack by active oxygen and nitrogen compounds. The tissue regeneration is regulated by a cascade of tyrosine protein kinases. Gastric ulceration leads to a decrease in activity of tyrosine protein kinases and phosphatases, following by fall in phosphotyrosine content in proteins of plasma membranes of gastric mucosa cells. No changes in superoxide dismutase activity, slight increase in catalase activity, inhibition of glutathione peroxydase, significant increase in OH* content and decrease in zinc level were observed in the gastric mucosa cells of stressed rats. That increased oxidative damage can lead to inactivation of protein tyrosine phosphatases. Nitric oxide synthase activity was three times higher in gastric mucosa cells after the cold stress. That can promote nitrosylation of tyrosine residues. During following days nitric oxide synthase activity remains high. Superoxide dismutase is activated on the 4 and 5th day after the stress. Catalase activity normalizes after second day. Tyrosine protein kinase activity increases in membranes with maximum on the 4th day, and remains inhibited in cytosole. Tyrosine protein phosphatases keep inhibited as well. Gluthatione peroxydase activity and zinc level decreased on the 5th day. Obtained results can be the evidence of violations in signal transduction through protein tyrosine kinase cascades, due to the reduction in tyrosine phosphorylation, as a result of increase in the content of active oxygen and nitrogen species.
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PMID:[Functioning of tyrosine protein kinases and phosphatases in gastric mucosa cells under conditions of oxidative and nitrosative stress in gastric lesions]. 1924 21

Zn(II)-curcumin, a mononuclear (1:1) zinc complex of curcumin was synthesized and examined for its antiulcer activities against pylorus-ligature-induced gastric ulcer in rats. The structure of Zn(II)-curcumin was identified by elemental analysis, NMR and TG-DTA analysis. It was found that a zinc atom was coordinated through the keto-enol group of curcumin along with one acetate group and one water molecule. Zn(II)-curcumin (12, 24 and 48 mg/kg) dose-dependently blocked gastric lesions, significantly reduced gastric volume, free acidity, total acidity and pepsin, compared with control group (P<0.001) and curcumin alone (24 mg/kg, P<0.05). Reverse transcriptase polymerase chain reaction (RT-PCR) analysis showed that Zn(II)-curcumin markedly inhibited the induction of nuclear factor-kappa B (NF-kappaB), transforming growth factor beta(1) (TGF-beta(1)) and interleukin-8 (IL-8), compared with control group (P<0.05). These findings suggested that Zn(II)-curcumin prevented pylorus-ligation-induced lesions in rat by inhibiting NF-kappaB activation and the subsequent production of proinflammatory cytokines, indicating a synergistic effect between curcumin and zinc. An acute toxicity study showed that mice treated with SDs of Zn(II)-curcumin (2 g/kg) manifested no abnormal signs.
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PMID:Gastroprotective effects of a new zinc(II)-curcumin complex against pylorus-ligature-induced gastric ulcer in rats. 1958 37

The aim of this retrospective study of patients with tongue pain who showed no improvement after initial treatment and examination was to find out if their lack of response correlated with serum concentrations of zinc, vitamin B12, folic acid, and copper, and if it was associated with coexisting systemic diseases. We studied 311 patients for whom we had data about serum concentrations of these elements, and recorded whether they had any systemic diseases and were taking medicines regularly. One patient (0.3%) had a copper concentration outside the reference range; 2 patients (0.6%) had folic acid concentrations outside the reference range. The corresponding number for vitamin B12 was 5 (2%), and for zinc 30 (10%). The systemic diseases with the highest rates were: hyperlipidaemia (n=53, 17%), gastritis or gastric ulcer (n=51, 16%), angina pectoris (n=39, 13%), diabetes mellitus (n=31, 10%), thyroid disease (n=31, 10%), mild mental disorder (n=27, 9%), hypertension (n=18, 6%), cerebral infarction (n=17, 6%), leiomyoma (n=15, 5%) and anaemia (n=15, 5%). Roughly 10% of the patients were deficient in zinc. This study suggested that the serum concentration of zinc was most important to the patients with tongue pain. Many patients had more than one systemic condition, and all were taking various drugs.
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PMID:Clinical study of tongue pain: Serum zinc, vitamin B12, folic acid, and copper concentrations, and systemic disease. 1973 64


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