Wyniki wyszukiwania

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Involvement of cyclooxygenase-1 and cyclooxygenase-2 activity in the therapeutic effect of ghrelin in the course of ethanol-induced gastric ulcers in rats

100%

Warzecha Z., Ceranowicz P., Dembinski M., Cieszkowski J., Ginter G., Ptak-Belowska A., Dembinski A.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 1

2

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The role of capsaicin - sensitive sensory neurons and nitric oxide in regulation of gastric mucosal growth

100%

Dembinski A., Warzecha Z., Ceranowicz P., Konturek S. J.

Journal of Physiology and Pharmacology

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1995

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tom 46

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nr 3

3

Acid-sensing protective mechanisms of duodenum

80%

Kaunitz J. D., Akiba Y.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 4

19-26

The proximal duodenal mucosa, exposed to frequent pulses of gastric acid, is functionally "leaky", increasing the importance of defense mechanisms such as the mucus gel layer, cellular acid/base transporters, bicarbonate secretion, and mucosal blood flow. Our laboratory has used a unique in vitro perfused microscopic system to measure thickness of the adherent mucus gel (MGT), intracellular pH (pHi), bicarbonate secretion, and mucosal blood flow in anesthetized rats. Exposure to pulses of luminal acid, mimicking the rapid physiologic shifts of luminal pH, increases MGT and blood flow, and induces cellular bicarbonate loading, the latter followed by augmented bicarbonate secretion. The mechanism by which the epithelium senses luminal acid includes capsazepine-inhibitable vanilloid receptors, presumably similar to the vanilloid receptor TPVR-1. CFTR, the cAMP-regulated anion channel mutated in the disease cystic fibrosis, plays an essential role in duodenal bicarbonate secretion. Our data are consistent with the hypothesis that cellular bicarbonate loading is an important means of preserving epithelial pHi during luminal acid challenge. Increased MGT may damp rapid shifts of luminal pH. Enhanced mucosal blood flow plays a significant role in the removal of back-diffusing acid. These neurally coordinated systems act coherently to defend the vulnerable duodenal epithelial cells from concentrated gastric acid.

4

Therapeutic effect of exogenous ghrelin in the healing of gingival ulcers is mediated by the release of endogenous growth hormone and insulin-like growth factor-1

80%

Cieszkowski J., Warzecha Z., Ceranowicz P., Ceranowicz D., Kusnierz-Cabala B., Pedziwiatr M., Dembinski M., Ambrozy T., Kaczmarzyk T., Pihut M., Wieckiewicz M., Olszanecki R., Dembinski A.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 4

5

Treatment with ghrelin accelerates the healing of acetic acid-induced gastric and duodenal ulcers in rats

80%

Ceranowicz P., Warzecha Z., Dembinski A., Sendur R., Cieszkowski J., Ceranowicz D., Pawlik W. W., Kuwahara A., Kato I., Konturek P. C.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 1

87-98

Recent studies have shown that ghrelin exhibits gastroprotective effects. The aim of present study was to examine the influence of ghrelin administration on the healing of chronic gastric and duodenal ulcers and to evaluate the role of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in this process. In pituitary-intact or hypophysectomized rats, chronic gastric and duodenal ulcers were induced by acetic acid. After induction of ulcers, rats were treated intraperitoneally twice a day with saline, ghrelin (4, 8 or 16 nmol/kg/dose) or IGF-1 (20 nmol/kg/dose) for six or ten days. In animals with intact pituitary, treatment with ghrelin increased serum level of GH and IGF-1. These effects were accompanied by the increase in mucosal cell proliferation, mucosal blood flow and healing rate of gastric and duodenal ulcers. After hypophysectomy, the significant increase in serum level of endogenous ghrelin was observed, but the healing of gastric and duodenal ulcers was delayed. This effect was accompanied by a significant decrease in serum concentration of endogenous GH and IGF-1, and reduction in mucosal blood flow and DNA synthesis. In hypophysectomized rats, administration of exogenous ghrelin was without any effect on serum level of GH and IGF-1, healing rate of gastroduodenal ulcers or mucosal cell proliferation. In contrast to this effect, administration of IGF-1 increased mucosal cell proliferation, healing rate of gastroduodenal ulcers and mucosal blood flow in hypophysectomized rats. Conclusion: Treatment with ghrelin accelerates healing of chronic gastroduodenal ulcers and this effect is mediated by the release of endogenous GH and IGF-1.

6

Characterization of antichemotactic factor extracted from the gastric mucosa of rats

80%

Fujita H., Takahashi S., Okabe S.

Journal of Physiology and Pharmacology

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1997

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tom 48

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nr 4

7

Lipopolysaccharide of Helicobacter pylori protects gastric mucosa via generation of nitric oxide

80%

Brzozowski T., Konturek P. C., Sliwowski Z., Drozdowicz D., Pajdo R., Stachura J., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology

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1997

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tom 48

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nr 4

Ograniczanie wyników

Involvement of cyclooxygenase-1 and cyclooxygenase-2 activity in the therapeutic effect of ghrelin in the course of ethanol-induced gastric ulcers in rats

The role of capsaicin - sensitive sensory neurons and nitric oxide in regulation of gastric mucosal growth

Acid-sensing protective mechanisms of duodenum

Therapeutic effect of exogenous ghrelin in the healing of gingival ulcers is mediated by the release of endogenous growth hormone and insulin-like growth factor-1

Treatment with ghrelin accelerates the healing of acetic acid-induced gastric and duodenal ulcers in rats

Characterization of antichemotactic factor extracted from the gastric mucosa of rats

Lipopolysaccharide of Helicobacter pylori protects gastric mucosa via generation of nitric oxide