Wyniki wyszukiwania

1

Influence of central and peripheral administration of pancreatic polypeptide on gastric mucosa growth

100%

Dembinski A., Warzecha Z., Ceranowicz P., Pawlik M., Dembinski M., Kabat K., Konturek S. J., Kownacki P., Hladki W., Pawlik W. W.

Journal of Physiology and Pharmacology

|

2004

|

tom 55

|

nr 1,2

Previous studies have shown that pancreatic polypeptide (PP) inhibits exocrine pancreatic secretion. The aim of present study was to determine the influence of PP administration on gastric growth and blood flow. Methods: Study was performed on regularly fed, fasted or fasted and subsequently refed rats. Rats were treated with saline (intraperitoneally - i.p.), caerulein (0.24 nmol/kg/dose, i.p.), pentagastrin (0.38 µmol/kg/dose, i.p.) or PP (5 nmol/kg/dose, i.p. or 10 pmol/dose intracerebroventricularly - i.c.v.). Saline, caerulein, pentagastrin and PP were administered alone or in combination, 3 times daily during last 48 h of experiment. Results: Treatment with pentagastrin increased gastric mucosa weight, mucosal DNA synthesis and gastric blood flow in all group tested. Intraperitoneal and i.c.v administration of PP alone reduced mucosal DNA synthesis in regularly fed and refed animals, and decreased gastric blood flow in refed animals. Combination of PP i.p. or i.c.v plus pentagastrin significantly reduced the pentagastrin-evoked increase in gastric mucosa weight, gastric DNA synthesis and gastric blood flow in fasted animals, as well as regularly fed animals. In refed animals, influence of PP administration on the pentagastrin-evoked increase in gastric mucosa weight was weak and statistically insignificant, but still i.p or i.c.v administration of PP significantly reduced gastric blood flow and mucosal DNA synthesis in this group of animals. Administration of caerulein caused weak, but significant increase in gastric DNA synthesis, gastric mucosa weight and gastric blood flow in fasted rats. In regularly fed animals, caerulein significantly increased only gastric DNA synthesis and gastric blood flow. In fasted animals with subsequent refeeding, caerulein was without effect on parameters tested in the stomach. Neither i.p. nor i.c.v administration of PP affected the caerulein-evoked effects in the stomach. Conclusions: Peripheral and central administration of PP inhibits food- and pentagastrin-stimulated growth of gastric mucosa. Similar effects of low central doses of PP as the high peripheral doses of PP suggests a crucial role of the central nervous system in the inhibitory effect of PP on gastric mucosa growth.

2

Sensory nerves and calcitonin gene related peptide in the effect of ischemic preconditioning on acute and chronic gastric lesions induced by ischemia-reperfusion

100%

Pawlik M., Ptak A., Pajdo R., Konturek P. C., Brzozowski T., Konturek S. J.

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 4,1

Ischemic preconditioning is considered as the most powerful gastroprotective intervention against mucosal lesions and ulcerations but the mechanism of this phenomenon has been little examined. In this study we tested the effects of inactivation of sensory nerves in new rat model combining acute gastric erosions with subsequent ulcers induced by ischemia-reperfusion (I/R). I/R lesions were produced in rats by clamping the celiac artery for 0.5 h followed by 3 h ofreperfusion in rats with intact or inactivated sensory nerves by pretreatment with capsaicin for two weeks before the I/R. The animals were killed at 0 and 3 h and 3 days after I/R and the area of gastric lesions was determined planimetrically, the gastric blood flow (GBF) by H2-gas clearance technique and the plasma levels of gastrin by RIA. Gastric mucosal content of calcitonin gene related peptide (CGRP) was assessed by RIA. Following I/R, gastric erosive lesions occurred after 3 h and these erosive lesions then progressed into gastric ulcers within 3 days in all rats. Sensory-inactivation with capsaicin caused several fold increase in the area of early (at 3 h) acute lesions and later (at 3 d) gastric ulcers induced by I/R. This enhancement of acute and then chronic gastric lesions was accompanied by a significant fall in GBF, an elevation of plasma gastrin and a decrease in mucosal expression of CGRP. Ischemic preconditioning markedly reduced acute lesions and chronic ulcerations induced by I/R and attenuated the changes in plasma gastrin and mucosal CGRP contents but these effects were significantly more pronounced in rats with intact sensory nerves but less in capsaicin-inactivated animals. We conclude that: 1) The I/R resulted in the formation of early acute gastric lesions followed 3 days later by chronic gastric ulcers and this gastric injury was accompanied by an impairment of gastric microcirculation, hypergastrinemia and suppression the gastric mucosal CGRP; 2) Gastric ischemic-preconditioning significantly attenuated both acute mucosal damage and chronic ulcers induced by I/R and this was accompanied by a rise in gastric blood flow; 3) The inactivation of sensory nerves with capsaicin enhanced the formation of I/R-induced acute and chronic gastric lesions and strongly attenuated the gastroprotection afforded by I/R possibly due to the decline in mucosal blood flow and the fall in expression of integrity peptides such as CGRP and 4) The excessive release of gastrin may limit the extent of mucosal lesions observed during progression of gastric erosions into ulcers induced by I/R.

3

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Nitric oxide is involved in the mediation of gastric blood flow and tissue oxygenation

100%

Gustaw P., Pawlik W. W., Czarnobilski K., Sendur R., Konturek S. J.

Journal of Physiology and Pharmacology

|

1994

|

tom 45

|

nr 3

4

The effect of hydrogen sulfide-releasing naproxen (ATB-346) versus naproxen on formation of stress-induced gastric lesions. The regulation of systemic inflammation, hypoxia and alterations in gastric microcirculation

84%

Magierowski M., Magierowska K., Surmiak M., Hubalewska-Mazgaj M., Kwiecien S., Wallace J. L., Brzozowski T.

Journal of Physiology and Pharmacology

|

2017

|

tom 68

|

nr 5

5

Involvement of cyclooxygenase (COX)-2 products in acceleration of ulcer healing by gastrin and hepatocyte growth factor

84%

Brzozowski T., Konturek P. C., Konturek S. J., Pajdo R., Schuppan D., Drozdowicz D., Ptak A., Pawlik M., Nakamura T., Hahn E. G.

Journal of Physiology and Pharmacology

|

2000

|

tom 51

|

nr 4,1

6

Role of histamine in regulation of blood flow in the injured gastric mucosa of the cat

84%

Gislason H., Svanes K.

Journal of Physiology and Pharmacology

|

1994

|

tom 45

|

nr 3

7

Brain-gut axis in gastroprotection by leptin and cholecystokinin against ischemia-reperfusion induced gastric lesions

84%

Brzozowski T., Konturek P. C., Pajdo R., Kwiecien S., Ptak A., Sliwowski Z., Drozdowicz D., Pawlik M., Konturek S. J., Hahn E. G.

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 4,1

Leptin, a product of ob gene controlling food intake, has recently been detected in the stomach and shown to be released by CCK and implicated in gastroprotection against various noxious agents but it is unknown whether centrally applied leptin influences ischemia-reperfusion (I/R)-induced gastric erosions that progress into deeper gastric ulcerations. In this study we compared the effects of leptin and CCK-8 applied intracerebroventricularly (i.c.v.) or intraperitoneally (i.p.) on gastric mucosal lesions induced by I/R and topical application of 75% ethanol. Several major series of Wistar rats were used to examine the effects of leptin and CCK applied centrally on gastroprotection against I/R and ethanol in rats with A) vagotomy by cutting of vagal nerves, B) suppression of NO-synthase with L-NNA (20 mg/kg i.p.), C) inactivation of sensory nerves by capsaicin (125 mg/kg s.c.) and D) inhibition of CGRP receptors with CGRP8-37 (100 µg/kg i.p.) applied with or without the i.c.v. pretreatment with leptin or CCK-8. Rats were anesthetized 1 h after ethanol administration or at 3 h and 3 days upon the end of ischemia to measure the gastric blood flow (GBF) and then to determine the area of gastric lesions by planimetry. Blood was withdrawn for the measurement of plasma leptin and gastrin levels by radioimmunoassay (RIA). Leptin (0.1—20 µg/kg i.p.) dose-dependently attenuated gastric lesions induced by 75% ethanol and I/R; the dose reducing these lesions by 50% (ED50) was 8 µg/kg and 6 µg/kg, respectively and this protective effect was similar to that obtained with CCK-8 applied in a standard dose of 10 µg/kg i.p. This protective effect of leptin was accompanied by a significant increase in GBF and plasma gastrin levels whereas CCK-8 increased plasma leptin levels but failed to affect plasma gastrin levels. Leptin and CCK-8 applied i.c.v. in a dose of 625 ng/rat reduced significantly the area of I/R induced gastric lesions and raised the GBF and plasma leptin levels with the extent similar to those achieved with peripheral administration of leptin or CCK-8 (10 µg/kg i.p.). The protective and hyperemic effects of centrally administered leptin or CCK-8 (625 ng/rat i.c.v.) were completely abolished by vagotomy and significantly attenuated by sensory denervation with capsaicin or by CGRP antagonist, CGRP8-37. The pretreatment with L-NNA to inhibit NO-synthase activity attenuated significantly the protective and hyperemic effects of CCK but not those of leptin while capsaicin denervation counteracted leptin-- induced protection and rise in the GBF but attenuated significantly those of CCK. We conclude that: 1) central leptin exerts a potent gastroprotective activity against I/R-induced gastric erosions that progress into deeper gastric lesions and this protection depends upon vagal activity and sensory nerves and involves hyperemia probably mediated by NO and 2) leptin mimics the gastroprotective effect of CCK and may be implicated in the protective and hyperemic actions of this peptide against mucosal damage evoked by I/R.

8

Importance of brain-gut axis in the gastroprotection induced by gastric and remote preconditioning

84%

Brzozowski T., Konturek P. C., Pajdo R., Kwiecien S., Sliwowski Z., Drozdowicz D., Ptak-Belowska A., Pawlik M., Konturek S. J., Pawlik W. W., Hahn E. G.

Journal of Physiology and Pharmacology

|

2004

|

tom 55

|

nr 1,2

Limitation of the damage to the organs such as heart, liver, intestine, stomach and brain by an earlier brief complete occlusion of their arteries is defined as ischemic preconditioning (IP). No study so for has been undertaken to check whether brain-gut axis is involved in the gastroprotection exhibited by gastric IP or in that induced by repeated brief episodes of ischemia of remote organs such as heart and liver. This study was designed to determine the possible involvement of vagal and sensory afferent nerves, in the mechanism of gastric and remote organ IP on the gastric mucosa in rats exposed to prolonged ischemia-reperfusion with or without functional ablation of sensory nerves by capsaicin or in those with removed vagal innervation by vagotomy. This gastric IP was induced by short ischemia episodes (occlusion of celiac artery 1-5 times for 5 min) applied 30 min before subsequent ischemia followed by 3 h of reperfusion (I/R) and compared with remote IP induced by occlusion of left descending coronary artery or hepatic artery plus portal vein. The area of gastric lesions was determined by planimetry, gastric blood flow (GBF) was measured by H2-gas clearance method and mucosal biopsy samples were taken for the assessment of calcitonin gene-related peptide (CGRP) by RIA. Exposure of gastric mucosa to standard 3 h of I/R produced numerous gastric lesions and significant fall in the GBF and mucosal CGRP content. Two 5 min short ischemic episodes by occlusion of coronary or hepatic arteries, significantly reduced gastric damage induced by I/R with the extent similar to that exhibited by two short (5 min) episodes of gastric ischemia. These protective effects of gastric and remote IPs were accompanied by a restoration of the fall in the CGRP content caused by I/R alone. Protection and hyperemia induced by gastric IP were significantly attenuated in capsaicin-denervated or vagotomized animals and completely removed in those exposed to the combination of vagotomy and capsaicin-denervation. The IP-induced protection and hyperemia were restored by the administration of exogenous CGRP to gastric IP in capsaicin-treated animals. Gastroprotective and hyperemic actions of remote IP were markedly diminished in capsaicin-denervated rats and in those subjected to vagotomy. We conclude that brief ischemia in remote organs such as heart and liver protects gastric mucosa against gastric injury induced by I/R as effectively as gastric IP via mechanism involving both vagal and sensory nerves releasing vasodilatatory mediators such as CGRP.

9

Apoptosis in gastric mucosa with stress-induced gastric ulcers

84%

Konturek P. C., Brzozowski T., Konturek S. J., Pajdo R., Konturek J. E., Kwiecien S., Taut A., Hahn E. G.

Journal of Physiology and Pharmacology

|

1999

|

tom 50

|

nr 2

10

SU-840, a novel synthetic flavonoid derivative of sophoradin, with potent gastroprotective and ulcer healing activity

84%

Brzozowski T., Konturek S. J., Kwiecien S., Pajdo R., Drozdowicz D., Sliwowski Z., Muramatsu M.

Journal of Physiology and Pharmacology

|

1998

|

tom 49

|

nr 1

11

Effect of local injection with basic fibroblast growth factor (BFGF) and neutralizing antibody to BFGF on gastric ulcer healing, gastric secretion, angiogenesis and gastric blood flow

84%

Ernst H., Konturek P. C., Hahn E. G., Stosiek H. P., Brzozowski T., Konturek S. J.

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 3

12

Nitric oxide (NO)-releasing aspirin and (NO) donors in protection of gastric mucosa against stress

84%

Kwiecien S., Pawlik M. W., Brzozowski T., Konturek P. C., Sliwowski Z., Pawlik W. W., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

|

2008

|

tom 59

|

nr 2

Acute gastric mucosal lesions represent an important clinical problem. The experimental model of acute gastritis such as water immersion restraint (WRS) stress is useful tool in examination of pathomechanism of acute gastric damage. Nitric oxide (NO) plays an important role in the maintenance of gastric barrier, however the role of reactive oxygen species (ROS) in the interaction between NO and gastric mucosa integrity has been little studied. The purpose of our present study was to explain the participation of ROS in healing of WRS-induced gastric lesions accelerated by NO. Experiments were carrying out on 120 male Wistar rats. To assess gastric blood flow (GBF) laser Doppler flowmeter was used. The number of gastric lesions was established by planimetry. The colorimetric assays were used to determine gastric tissue level of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), the products of lipid peroxidation by ROS, as well as superoxide dismutase (SOD) activity, the enzyme scavanger of ROS. We demonstrated that 3.5 h of WRS resulted in appearance of acute gastric mucosal lesions accompanied by a significant decrease of GBF. Biological effects of ROS were estimated by measuring tissue level of MDA and 4-HNE, as well as the SOD activity. It was demonstrated that 3.5 h of WRS led to significant increase of MDA and 4-HNE mucosal level, that was accompanied by a decrease of SOD activity. Pretreatment with NO-donors (SIN-1, SNAP, nitroglycerin, NO-ASA) resulted in reduction of gastric lesions number, increment of GBF, decrease of MDA and 4-HNE tissue level and increase of SOD activity. Suppression of ROS play an important role in NO-donors action in gastroprotection against gastric acute lesions induced by 3.5 h of WRS. NO-donors cause an attenuation of lipid peroxidation as documented by a decrease of MDA and 4-HNE levels and enhancement of antioxidative properties as evidenced by increase of SOD activity.

13

Role of prostaglandins in gastroprotection and gastric adaptation

67%

Brzozowski T., Konturek P. C., Konturek S. J., Brzozowska I., Pawlik T.

Journal of Physiology and Pharmacology. Supplement

|

2005

|

tom 56

|

nr 5

33-55

Since Robert discovery that pretreatment with prostaglandin (PG) applied in non-antisecretory dose can prevent the injury of gastric mucosa induced by necrotizing agents, much attention was paid to the role of these cyclooxygenaxe (COX) products in the mechanism of gastric mucosal integrity and ulcer healing. The ability of exogenous PG to attenuate or even completely prevent mucosal damage caused by corrosive substances such as absolute ethanol, hiperosmolar solutions or concentrated bile has been termed "cytoprotection". Increased generation of endogenous PG in the gastric mucosa exposed to the topical contact with "mild irritant" such as 20% ethanol, 1 mM NaCl or 5 mM taurocholate also prevented gastric injury caused by strong irritants via phenomenon of adaptive cytoprotection. Other mediators such as growth factors, nitric oxide (NO) or calcitonin gene related peptide (CGRP) as well as some gut hormones including gastrin and cholecystokinin (CCK), leptin, ghrelin and gastrin-releasing peptide (GRP) have been also found to protect gastric mucosa against the damage induced by corrosive substances. This protective action of gut hormones has been attributed to the release of PG or activation of sensory nerves because it could be abolished by the pretreatment with indomethacin or large neurotoxic dose of capsaicin and restored by the addition of exogenous PGE2 or CGRP, respectively. Short (5 min) ischemia of the stomach applied before prolonged ischemia-reperfusion (I/R) attenuated markedly the gastric lesions produced by this I/R and also prevented the mucosal damage provoked by necrotizing substances. This protection could be abolished by the pretreatment with non-steroidal anti-inflammatory drugs (NSAID) and was accompanied by an enhamcement of gastric mucosal COX-2 expression and activity. Exposure of gastric mucosa to single insult of acidified aspirin (ASA) causes severe mucosal damage with occurence of multiple haemorrhagic lesions but with repeated application of ASA, the attenuation of mucosal lesions is observed, despite the profound inhibition of PGE2 generation. This phenomenon called "gastric adaptation" does not appear to depend upon endogenous biosynthesis of PG but possibly involves enhanced production of growth factors increasing cell proliferation and mucosal regeneration. Unlike short lived gastroprotection by PG, NO, CGRP, mild irritants or short ischemia, gastric adaptation appears to be long-lasting phenomenon accompanied by increased resistance of the adapted mucosa to subsequent damage induced by corrosive agents.

14

Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense

67%

Brzozowska I., Ptak-Belowska A., Pawlik M., Bajdo R., Drozdowicz D., Konturek S. J., Pawlik W. W., Brzozowski T.

Journal of Physiology and Pharmacology. Supplement

|

2009

|

tom 60

|

nr 7

15

Importance of luminal and mucosal zinc in the mechanism of experimental gastric ulcer healing

67%

Opoka W., Adamek D., Plonka M., Reczynski W., Bas B., Drozdowicz D., Jagielski P., Sliwowski Z., Adamski P., Brzozowski T.

Journal of Physiology and Pharmacology

|

2010

|

tom 61

|

nr 5

16

Experimental healing of preexisting gastric ulcers induced by hormones controlling food intake ghrelin, orexin-A and nesfatin-1 is impaired under diabetic conditions. A key to understanding the diabetic gastropathy?

67%

Szlachcic A., Majka J., Strzalka M., Szmyd J., Pajdo R., Ptak-Belowska A., Kwiecien S., Brzozowski T.

Journal of Physiology and Pharmacology

|

2013

|

tom 64

|

nr 5

17

The renin-angiotensin system and its vasoactive metabolite angiotensin-(1-7) in the mechanism of the healing of preexisting gastric ulcers. The involvement of mas receptors, nitric oxide, prostaglandins and proinflammatory cytokines

67%

Pawlik M. W., Kwiecien S., Ptak-Bielowska A., Pajdo R., Olszanecki R., Suski M., Madej J., Targosz A., Konturek S. J., Korbut R., Brzozowski T.

Journal of Physiology and Pharmacology

|

2016

|

tom 67

|

nr 1

18

Role of sensory afferent nerves, lipid peroxidation and antioxidative enzymes in the carbon monoxide-induced gastroprotection against stress ulcerogensis

67%

Kwiecien S., Magierowska K., Magierowski M., Surmiak M., Hubalewska-Mazgaj M., Pajdo R., Sliwowski Z., Chmura A., Wojcik D., Brzozowski T.

Journal of Physiology and Pharmacology

|

2016

|

tom 67

|

nr 5

19

Gastroprotection and control of food intake by leptin. Comparison with cholecystokinin and prostaglandins

67%

Konturek P. C., Konturek S. J., Brzozowski T., Hahn E. G.

Journal of Physiology and Pharmacology

|

1999

|

tom 50

|

nr 1

20

Helicobacter pylori and gastric adaptation to repeated aspirin administration in humans

67%

Konturek J. W., Dembinski A., Konturek S. J., Domschke W.

Journal of Physiology and Pharmacology

|

1997

|

tom 48

|

nr 3

Ograniczanie wyników

Influence of central and peripheral administration of pancreatic polypeptide on gastric mucosa growth

Sensory nerves and calcitonin gene related peptide in the effect of ischemic preconditioning on acute and chronic gastric lesions induced by ischemia-reperfusion

Nitric oxide is involved in the mediation of gastric blood flow and tissue oxygenation

The effect of hydrogen sulfide-releasing naproxen (ATB-346) versus naproxen on formation of stress-induced gastric lesions. The regulation of systemic inflammation, hypoxia and alterations in gastric microcirculation

Involvement of cyclooxygenase (COX)-2 products in acceleration of ulcer healing by gastrin and hepatocyte growth factor

Role of histamine in regulation of blood flow in the injured gastric mucosa of the cat

Brain-gut axis in gastroprotection by leptin and cholecystokinin against ischemia-reperfusion induced gastric lesions

Importance of brain-gut axis in the gastroprotection induced by gastric and remote preconditioning

Apoptosis in gastric mucosa with stress-induced gastric ulcers

SU-840, a novel synthetic flavonoid derivative of sophoradin, with potent gastroprotective and ulcer healing activity

Effect of local injection with basic fibroblast growth factor (BFGF) and neutralizing antibody to BFGF on gastric ulcer healing, gastric secretion, angiogenesis and gastric blood flow

Nitric oxide (NO)-releasing aspirin and (NO) donors in protection of gastric mucosa against stress

Role of prostaglandins in gastroprotection and gastric adaptation

Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense

Importance of luminal and mucosal zinc in the mechanism of experimental gastric ulcer healing

Experimental healing of preexisting gastric ulcers induced by hormones controlling food intake ghrelin, orexin-A and nesfatin-1 is impaired under diabetic conditions. A key to understanding the diabetic gastropathy?

The renin-angiotensin system and its vasoactive metabolite angiotensin-(1-7) in the mechanism of the healing of preexisting gastric ulcers. The involvement of mas receptors, nitric oxide, prostaglandins and proinflammatory cytokines

Role of sensory afferent nerves, lipid peroxidation and antioxidative enzymes in the carbon monoxide-induced gastroprotection against stress ulcerogensis

Gastroprotection and control of food intake by leptin. Comparison with cholecystokinin and prostaglandins

Helicobacter pylori and gastric adaptation to repeated aspirin administration in humans