Wyniki wyszukiwania

1

Grelina – hormon żarłoczności?

100%

Dembinski A., Warzecha Z.

Kosmos

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2010

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tom 59

|

nr 3-4

2

Peptidyl hormones of endocrine cells origin in the gut - their discovery and physiological relevance

81%

Ceranowicz P., Warzecha Z., Dembinski A.

Journal of Physiology and Pharmacology

|

2015

|

tom 66

|

nr 1

3

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

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

81%

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

4

The effects of antagonists of receptors for gastrin, cholecystokinin and bombesin on growth of gastroduodenal mucosa and pancreas

71%

Dembinski A., Warzecha Z., Konturek S. J., Zhi Cai R., Schally A. V.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 2

The effects of gastrin, cholecystojdnin (CCK) and bombesin on the DNA synthesis, as a biochemical indicator of trophic action in the gastroduodenal mucosa and the pancreas have been examined in rats fasted for 48 h and in rats refed for 16 h with or without administration of specific receptor antagonists for bombesin, gastrin and CCK. Bombesin and gastrin administered three times daily for 48 h in fasted rats significantly increased the rate of DNA synthesis as measured by the incorporation of [³H] thymidine into DNA in each tissue tested. CCK significantly increased DNA synthesis in the duodenal mucosa and pancreatic tissue, but not in the gastric mucosa. The stimulation of DNA synthesis induced by bombesin in the gastroduodenal mucosa and pancreas was abolished by bombesin/GRP receptor antagonist, RC-3095. RC-3095 did not affect DNA synthesis stimulated by gastrin and CCK in these tissues. L-365,260, a receptor antagonist for gastrin suppressed the DNA synthesis induced by gastrin but not by CCK or bombesin in the gastrointestinal mucosa and pancreas. L-364, 718 a specific antagonist for CCK receptors was effective only against CCK stimulated duodenal mucosa and pancreatic growth. Refeeding of 48 h fasting rats strongly enhanced the DNA synthesis in all tissues tested, and this effect was significantly reduced in the gastroduodenal mucosa by blocking only gastrin receptors (with L-365, 260) and that in the duodenal mucosa and the pancreas by antagonizing of CCK receptors (with L-364, 718). Antagonism of bombesin receptors (with RC-3095) did not significantly affect the stimulation of DNA synthesis induced by refeeding in all tissues tested. This study indicates that the stimulation of DNA synthesis can be achieved by exogenous gastrin, CCK and bombesin acting through separate receptor but that only gastrin and CCK play the major role in the postprandial stimulation of the growth of gastroduodenal mucosa and pancreatic tissue.

5

Influence of sensory nerves and CGRP on the course of experimental pancreatitis and pancreatic regeneration

71%

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

Journal of Physiology and Pharmacology. Supplement

|

2001

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tom 52

|

nr 2

6

Ghrelin accelerates the healing of oral ulcers in non-sialoadenectomized and in sialoadenectomized rats

61%

Warzecha Z., Kownacki P., Ceranowicz P., Dembinski M., Cieszkowski J., Dembinski A.

Journal of Physiology and Pharmacology

|

2013

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tom 64

|

nr 5

7

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

61%

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

Journal of Physiology and Pharmacology

|

2014

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tom 65

|

nr 1

8

The effect of antagonist of receptors for gastrin, cholecystokinin and bombesin on growth of gastroduodenal mucosa and pancreas

61%

Dembinski A., Warzecha Z., Konturek S. J., Banas M., Cai R.-Z., Schally A. V.

Journal of Physiology and Pharmacology

|

1991

|

tom 42

|

nr 3

The effects of gastrin, cholecystokinin (CCK) and bombesin on the DNA synthesis, as a biochemical indicator of trophic action in the gastroduodenal mucosa and the pancreas, have been examined in rats fasted for 48 h and in rats refed for 16 h with or without administration of specific receptor antagonists for bombesin, gastrin and CCK. Bombesin and gastrin administered three times daily for 48 h in fasted rats significantly increased the rate of DNA synthesis as measured by the incorporation of [³H] thymidine into DNA in each tissue tested. CCK significantly increased DNA synthesis in the duodenal mucosa and pancreatic tissue, but not in the gastric mucosa. The stimulation of DNA synthesis induced by bombesin in the gastroduodenal mucosa and pancreas was abolished by bombesin/GRP receptor antagonist, RC-3095. RC-3095 did not affect DNA synthesis stimulated by gastrin and CCK in these tissues. L-365,260, a receptor antagonist for gastrin suppressed the DNA synthesis induced by gastrin but not by CCK or bombesin in the gastrointestinal mucosa and pancreas. L-364,718, a specific antagonist for CCK receptors was effective only against CCK stimulated duodenal mucosa and pancreatic growth. Refeeding of 48 h fasting rats strongly enhanced the DNA synthesis in all tissues tested, and this effect was significantly reduced in the gastroduodenal mucosa by blocking only gastrin receptors (with L-365, 260) and that in the duodenal mucosa and the pancreas by antagonizing of CCK receptors (with L-364, 718). Antagonism of bombesin receptors (with RC-3095) did not significantly affect the stimulation of DNA synthesis induced by refeeding in all tissues tested. This study indicates that the stimulation of DNA synthesis can be achieved by exogenous gastrin, CCK and bombesin acting through separate receptors, but that only gastrin and CCK play the major role in the postprandial stimulation of the growth of gastroduodenal mucosa and pancreatic tissue.

9

Role of sensory nerves in gastroprotective effect of anandamide in rats

61%

Warzecha Z., Dembinski A., Ceranowicz P., Dembinski M., Cieszkowski J., Kownacki P., Konturek P. C.

Journal of Physiology and Pharmacology

|

2011

|

tom 62

|

nr 2

Previous studies have shown that stimulation of cannabinoid 1 (CB1) receptor protects the gastric mucosa against stress-induced lesion. Aim of the present study was to examine the influence of anandamide on lipid peroxidation and antioxidant defense system in gastric mucosa and the role of sensory nerves in gastroprotective effects of cannabinoids. Studies were performed on rats with intact or ablated sensory nerves (by neurotoxic doses of capsaicin). Gastric lesions were induced by water immersion and restrain stress (WRS). Anandamide was administered at the dose of 0.3, 1.5 or 3.0 µmol/kg, 30 min before exposure to WRS. CB1 receptor antagonist, AM251 (4.0 µmol/kg) was administered 40 min before WRS. WRS induced gastric lesions associated with the decrease in gastric blood flow, mucosal DNA synthesis and mucosal activity of superoxide dismutase (SOD). Serum level of interleukin-1ß (IL-1ß) and mucosal level of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) were increased. Administration of anandamide reduced the ulcers area, generation of MDA+4-HNE and serum level of IL-1ß, and this effect was associated with the reduction in the WRS-induced decrease in gastric mucosal blood flow, mucosal DNA synthesis and SOD activity. Ablation of sensory nerves increased the area of ulcers, serum level of IL-1ß and mucosal content of MDA+4-HNE, whereas mucosal DNA synthesis, SOD activity and blood flow were additionally decreased. In rats with ablation of sensory nerves, administration of anandamide at the high doses (1.5 and 3.0 µmol/kg) partly reduced deleterious effect of WRS on gastric mucosa, but this effect was weaker than in animals with intact sensory nerves. Low dose of anandamide (0.3 µmol/kg) was ineffective in the protection of gastric mucosa against the WRS-induced lesions in rats with ablation of sensory nerves. In rats with intact sensory nerves and exposed to WRS, administration of AM251 exhibited deleterious effect. In rats with ablation of sensory nerves and exposed to WRS, AM251 failed to affect mucosal injury in the stomach. We conclude that anandamide reduces the mucosal oxidative stress and exhibits gastroprotective effect against WRS-induced ulcers. These effects are partly mediated by sensory nerves.

10

Administration of warfarin accelerates the recovery in ischemia/reperfusion-induced acute pancreatitis

61%

Maduzia D., Ceranowicz P., Cieszkowski J., Chmura A., Galazka K., Kusnierz-Cabala B., Warzecha Z.

Journal of Physiology and Pharmacology

|

2020

|

tom 71

|

nr 3

11

Stimulation of sensory nerves and CGRP administration attenuates development pancreatitis evoked by ischemia-reperfusion

61%

Warzecha Z., Dembinski A., Ceranowicz P., Sendur R., Pawlik W. W., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

|

2001

|

tom 52

|

nr 2

12

Effect of sensory nerves and CGRP on the development of caerulein-induced pancreatitis and pancreatic recovery

61%

Warzecha Z., Dembinski A., Ceranowicz P., Stachura J., Tomaszewska R., Konturek S. J.

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 4,1

The function of primary sensory neurons is to receive and transmit information from external environment and these neurons are able to release neuromediators from the activated peripheral endings. The aim of this study was to determine the influence of sensory nerves and administration of their mediator — calcitonin gene related peptide (CGRP) on the course of acute pancreatitis (AP). Ablation of sensory nerves was performed by neurotoxic dose of capsaicin (100 mg/kg). Single or repeated episodes of AP were induced by caerulein infusion (10 µg/kg/h for 5 h). Five repeated AP were performed once a week. Capsaicin at the dose which stimulates sensory nerves (0.5 mg/kg/dose) or CGRP (10 µg/kg/dose) was administrated before and during or after single induction of AP, as well as, after each induction of repeated AP. Rats were killed at the time 0, 3 or 9 h after single induction of AP or two weeks after last induction of repeated AP. Ablation of sensory nerves aggravated pancreatic damage in caerulein-induced AP. Treatment with stimulatory doses of capsaicin or CGRP before and during single induction of AP attenuated the pancreatic damage in morphological examination. This effect was also manifested by partial reversion of AP evoked drop in DNA synthesis and pancreatic blood flow (PBF). Administration of CGRP after single AP induction aggravated histologically manifested pancreatic damage. The further decrease in PBF and DNA synthesis was also observed. Animals with five episodes of AP showed almost full pancreatic recovery two weeks after last induction of AP concerning all parameters tested. In stimulatory doses of capsaicin treated rats, we observed the decrease in pancreatic amylase and fecal chymotrypsin activity, as well as, the drop in DNA synthesis. Similar but less pronounced effects were observed after treatment with CGRP. We conclude that effect of sensory nerves and CGRP on AP is two-phase and time dependent. Stimulation of sensory nerves or the administration of CGRP during development of AP exhibits protective effects against pancreatic damage induced by caerulein overstimulation. After induction of AP, persistent activity of sensory nerves and presence of CGRP aggravate pancreatic damage and lead to functional insufficiency typical for chronic pancreatitis.

13

Expression of transforming growth factor-beta1 and epidermal growth factor in caerulein-induced pancreatitis in rat

61%

Konturek P. C., Dembinski A., Warzecha Z., Ceranowicz P., Konturek S. J., Stachura J., Hahn E. G.

Journal of Physiology and Pharmacology

|

1997

|

tom 48

|

nr 1

14

Role of sensory nerves in pancreatic secretion and caerulein - induced pancreatitis

61%

Warzecha Z., Dembinski A., Jaworek J., Ceranowicz P., Szlachcic A., Walocha J., Konturek S. J.

Journal of Physiology and Pharmacology

|

1997

|

tom 48

|

nr 1

15

The influence of epidermal growth factor on the course of ischemia-reperfusion induced pancreatitis in rats

61%

Tomaszewska R., Dembinski A., Warzecha Z., Ceranowicz P., Konturek S. J., Stachura J.

Journal of Physiology and Pharmacology

|

2002

|

tom 53

|

nr 2

Acute pancreatitis is accompanied by the enhanced expression of EGF in the pancreas and the administration of EGF was found to exhibit the beneficial effect on edematous cerulein-induced pancreatitis. Therefore, we decided to determine the influence of EGF on necro-hemorrhagic pancreatitis induced by ischemia and reperfusion (I/R). Acute pancreatitis was induced in rats by restricting the pancreatic blood flow (PBF) in the inferior splenic artery for 30 min using microvascular clips. EGF was administered three times daily (10µg/kg per dose s.c.) starting immediately after the clips removal. Rats were sacrificed on day 1, 3, 5, 10 and 21 following ischemia. PBF was measured using a laser Doppler flowmeter. Morphological signs of pancreatitis, as well as the levels of plasma amylase, lipase, interleukin-1ß and interleukin-10 concentration and pancreatic cell proliferation were examined. Results: Ischemia with reperfusion caused acute necro-hemorrhagic pancreatitis with a histological and biochemical manifestation of pancreatic damage, followed by a spontaneous regeneration. The administration of EGF caused the reduction in the histological signs of pancreatic damage, such as necrosis, edema and leukocyte infiltration, and accelerated the pancreatic repair. Also, EGF treatment significantly attenuated the reduction in pancreatic blood flow and DNA synthesis. The activity of plasma amylase and lipase, as well as plasma interleukin-1ß and interleukin-10 concentrations were decreased in EGF treated animals. Conclusions: EGF exerts beneficial influence on the course of I/R induced pancreatitis and this effect seems to be related to the reduction in the activation of pro-inflammatory interleukin cascade, the improvement of PBF, and the increase in pancreatic cell growth.

16

Ghrelin attenuates the development of acute pancreatitis in rats

61%

Dembinski A., Warzecha Z., Ceranowicz P., Tomaszewska R., Stachura J., Konturek S. J., Konturek P. C.

Journal of Physiology and Pharmacology

|

2003

|

tom 54

|

nr 4

Ghrelin, a circulating growth hormone-releasing peptide isolated from human and rat stomach, stimulates growth hormone secretion, food intake and exhibits gastroprotective properties. Ghrelin is predominantly produced by a population of endocrine cells in the gastric mucosa, but its presence in bowel, pancreas, pituitary and hypothalamus has been reported. In human fetal pancreas, ghrelin is expressed in a prominent endocrine cell population. In adult pancreatic islets the population of these cell is reduced. The aim of present study was to investigate the influence of ghrelin administration on the development of acute pancreatitis. Methods: Acute pancreatitis was induced in rat by caerulein injection. Ghrelin was administrated twice (30 min prior to the first caerulein or saline injection and 3 h later) at the doses: 2, 10 or 20 nmol/kg. Immediately after cessation of caerulein or saline injections the following parameters were measured: pancreatic blood flow, plasma lipase activity, plasma interleukin-1ß (IL-1ß) and interleukin 10 (IL-10) concentration, pancreatic DNA synthesis, and morphological signs of pancreatitis. Results: Administration of ghrelin without induction of pancreatitis did not affect significantly any parameter tested. Caerulein led to the development of acute edematous pancreatitis. Treatment with ghrelin at the dose 2 nmol/kg, during induction of pancreatitis, was without effect on pancreatic histology or biochemical and functional parameters. Treatment with ghrelin at the dose 10 and 20 nmol/kg attenuated the development of pancreatitis and the effects of both doses were similar. Administration of ghrelin (10 or 20 nmol/kg) reduced inflammatory infiltration of pancreatic tissue and vacuolization of acinar cells. Also, plasma lipase activity and plasma IL-1ß concentration were reduced, and caerulein-induced fall in pancreatic DNA synthesis was reversed. Administration of ghrelin at the dose 10 and 20 nmol/kg was without effect on caerulein-induced pancreatic edema and pancreatitis-related fall in pancreatic blood flow. Conclusions: (1) Administration of ghrelin attenuates pancreatic damage in caerulein-induced pancreatitis; (2) Protective effect of ghrelin administration seems to be related the inhibition in inflammatory process and the reduction in liberation of pro-inflammatory IL-1ß.

17

Calcitonin gene-related peptide can attenuate or augment pancreatic damage in caerulein-induced pancreatitis in rats

61%

Warzecha Z., Dembinski A., Ceranowicz P., Konturek P. C., Stachura J., Tomaszewska R., Konturek S. J.

Journal of Physiology and Pharmacology

|

1999

|

tom 50

|

nr 1

18

Histamine in stress ulcer prophylaxis in rats

61%

Warzecha Z., Dembinski A., Brzozowski T., Ceranowicz P., Dembinski M., Stachura J., Konturek S. J.

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 3

19

Platelet activating factor [PAF] inhibitor [TCV-309] reduces caerulein - and PAF-induced pancreatitis. A morphologic and functional study in the rat

61%

Tomaszewska R., Dembinski A., Warzecha Z., Banas M., Konturek S. J., Stachura J.

Journal of Physiology and Pharmacology

|

1992

|

tom 43

|

nr 4

Caerulein-induced acute pancreatitis was studied in rats. Consistent with this type of acute pancreatitis morphological (edema, leukocytic infiltration and acinar cell vaculization) and biochemical (increase in pancreatic protein content, PAF release and serum amylase) changes developed 5 hours after caerulein administration. In addition increase in pancreatic weight and decrease in pancreatic blood flow were noticed. PAF administration caused pancreatic damage similar in some parameters to caerulein-induced pancreatitis, along with reduction of pancreatic blood flow, increase in pancreatic protein content, and serum amylase. TCV-309, a selective PAF antagonist, administered prior to caerulein and/or PAF, reduced caerulein-induced pancreatitis and prevented PAF-induced pancreatitis. Results of our present studies indicate the crucial role of PAF in pathogenesis of experimental acute pancreatitis.

20

IGF-1 stimulates production of interleukin-10 and inhibits development of caerulein-induced pancreatitis

61%

Warzecha Z., Dembinski A., Ceranowicz P., Konturek S. J., Tomaszewska R., Stachura J., Konturek P. C.

Journal of Physiology and Pharmacology

|

2003

|

tom 54

|

nr 4

Insulin-like growth factor-1 (IGF-1) and other growth factors overexpression was reported in acute pancreatitis. Previous studies have shown the protective effect of epidermal growth factor (EGF), Hepatocyte Growth Factor (HGF) and Fibroblast Growth Factor (FGF) in the course of experimental acute pancreatitis. The aim of our studies was to determine the effect of IGF-1 administration on the development of caerulein-induced pancreatitis. Methods: Acute pancreatitis was induced by infusion of caerulein (10 µg/kg/h) for 5 h. IGF-1 was administrated twice at the doses: 2, 10, 50, or 100 µg/kg s.c. Results: Administration of IGF-1 without induction of pancreatitis increased plasma interleukin-10 (IL-10). Infusion of caerulein led to development of acute edematous pancreatitis. Histological examination showed pancreatic edema, leukocyte infiltration and vacuolization of acinar cells. Also, acute pancreatitis led to an increase in plasma lipase and interleukin 1ß (IL-1ß) level, whereas pancreatic DNA synthesis and pancreatic blood flow were decreased. Treatment with IGF-1, during induction of pancreatitis, increased plasma IL-10 and attenuated the pancreatic damage, what was manifested by histological improvement of pancreatic integrity, the partial reversion of the drop in pancreatic DNA synthesis and pancreatic blood flow, and the reduction in pancreatitis-evoked increase in plasma amylase, lipase and IL-1ß level. Protective effect of IGF-1 administration was dose-dependent. Similar strong protective effect was observed after IGF-1 at the dose 2 x 50 and 2 x 100 µg/kg. Conclusions: (1) Administration of IGF-1 attenuates pancreatic damage in caerulein-induced pancreatitis; (2) This effect is related, at least in part, to the increase in IL-10 production, the reduction in liberation of IL-1ß and the improvement of pancreatic blood flow.

Ograniczanie wyników

Grelina – hormon żarłoczności?

Peptidyl hormones of endocrine cells origin in the gut - their discovery and physiological relevance

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

The effects of antagonists of receptors for gastrin, cholecystokinin and bombesin on growth of gastroduodenal mucosa and pancreas

Influence of sensory nerves and CGRP on the course of experimental pancreatitis and pancreatic regeneration

Ghrelin accelerates the healing of oral ulcers in non-sialoadenectomized and in sialoadenectomized rats

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 effect of antagonist of receptors for gastrin, cholecystokinin and bombesin on growth of gastroduodenal mucosa and pancreas

Role of sensory nerves in gastroprotective effect of anandamide in rats

Administration of warfarin accelerates the recovery in ischemia/reperfusion-induced acute pancreatitis

Stimulation of sensory nerves and CGRP administration attenuates development pancreatitis evoked by ischemia-reperfusion

Effect of sensory nerves and CGRP on the development of caerulein-induced pancreatitis and pancreatic recovery

Expression of transforming growth factor-beta1 and epidermal growth factor in caerulein-induced pancreatitis in rat

Role of sensory nerves in pancreatic secretion and caerulein - induced pancreatitis

The influence of epidermal growth factor on the course of ischemia-reperfusion induced pancreatitis in rats

Ghrelin attenuates the development of acute pancreatitis in rats

Calcitonin gene-related peptide can attenuate or augment pancreatic damage in caerulein-induced pancreatitis in rats

Histamine in stress ulcer prophylaxis in rats

Platelet activating factor [PAF] inhibitor [TCV-309] reduces caerulein - and PAF-induced pancreatitis. A morphologic and functional study in the rat

IGF-1 stimulates production of interleukin-10 and inhibits development of caerulein-induced pancreatitis