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  1. 36 Journal of Physiology and Pharmacology

  2. 7 Journal of Physiology and Pharmacology. Supplement

  3. 2 Archivum Immunologiae et Therapiae Experimentalis

  4. 1 Bulletin of the Polish Academy of Sciences. Biological Sciences

  5. 1 Bulletin of the Veterinary Institute in Puławy

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  1. 13 Konturek S. J.

  2. 10 Brzozowski T.

  3. 10 Konturek P. C.

  4. 6 Konturek J. W.

  5. 6 Kwiecien S.

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  1. 1 2021

  2. 1 2019

  3. 2 2018

  4. 2 2017

  5. 1 2016

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1

Helicobacter pylori and gastric adaptation to repeated aspirin administration in humans

100%
Konturek J. W., Dembinski A., Konturek S. J., Domschke W.
Journal of Physiology and Pharmacology. Supplement
|
1997
|
tom 48
|
nr 1
2
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Content available

Heat shock protein 70 (HSP70) in gastric adaptation to aspirin in Helicobacter pylori infection

100%
Konturek J. W., Fischer H., Konturek P. C., Huber V., Boknik P., Luess H., Neumann J., Brzozowski T., Schmitz W., Hahn E. G., Domschke W., Konturek S. J.
Journal of Physiology and Pharmacology
|
2001
|
tom 52
|
nr 1
3

Expression profile analysis of human peripheral blood mononuclear cells in response to aspirin

100%
Choi S., Park H. S., Cheon M. S., Lee K.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
tom 53
|
nr 2
4
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Melatonin and its precursors L-tryptophan prevent acute gastric mucosal damage induced by aspirin in humans

100%
Konturek P. C., Celinski K., Slomka M., Cichoz-Lach H., Burnat G., Naegel A., Bielanski W., Konturek J. W., Konturek S. J.
Journal of Physiology and Pharmacology. Supplement
|
2008
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tom 59
|
nr 2
Melatonin (MT) and its precursor L-tryptophan (Trp) are implicated in the protection of gastric mucosa against noxious agents. However, the role of MT and Trp on the gastric mucosal injury induced by aspirin (ASA) in human has not been investigated. Studies in animals showed that both MT and Trp given intragastrically prevents the formation of gastric mucosal lesions induced by ASA. The aim of the present study was to determine the influence of MT and Trp given orally to healthy humans on gastric mucosal lesions induced by ASA. The present study included 21 healthy, Hp-negative male volunteers with intact gastro-duodenal mucosa aging 20-50 yr. They were divided in 3 groups; group1: 7 volunteers receiving daily 2 x 1g ASA (Polfa, Rzeszow) during 11 days; group 2: 7 healthy volunteers receiving 2x1g ASA and MT (Lekam, Zakroczyn) (5 mg 30 min prior to ASA) during 11 days and group 3: 7 healthy volunteers receiving 2x1g ASA and Trp (Ardeytropin, Germany) (0.5 g 30 min prior to ASA) during 11 days. Mucosal damage was evaluated at 3rd, 7th and 11th days of ASA administration by endoscopy using Lanza score. Plasma melatonin was measured using RIA and gastric mucosal generation of PGE2 was assessed also by RIA. ASA caused marked mucosal injury at all days of its administration except day 11th when only moderate lesions were evident. Pre-treatment with MT or Trp alone was accompanied by a significant decrease in gastric mucosal lesion score. Gastric mucosal generation of PGE2 was suppressed by about 90% in subjects treated with ASA without or with MT or Trp. We concluded that: MT and its precursor Trp significantly attenuate gastric mucosal lesions induced by aspirin. The action of Trp may be be mediated by MT produced in gastrointestinal tract from Trp. The gastroprotective action of MT and Trp is independent on gastric mucosal PGE2 generation.
5
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Delay in oral mucosal ulcer healing by aspirin is linked to the disturbances in p38 mitogen-activated protein kinase activation

100%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
|
2001
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tom 52
|
nr 2
6

Lipoxins and aspirin-triggered 15-epi-lipoxins are endogenous components of antiinflammation: Emergence of the counterregulatory side

84%
Serhan C. N.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
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tom 49
|
nr 3
177-188
7
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Prophylactic effect of egualen sodium, a stable azulene derivative, on gastrointestinal damage induced by ischemia-reperfusion, double antiplatelet therapy and loxoprofen in rats

84%
Amagase K., Yoshida Y., Hara D., Murakami T., Takeuchi K.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 1
8
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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
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2017
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tom 68
|
nr 5
9
Content available remote

Association between microvesicles bearing monomeric C-reactive protein and platelet reactivity. Relationship with low response to antiplatelet drugs?

84%
Siennicka A.
Journal of Physiology and Pharmacology
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2021
|
tom 72
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nr 1
10
Content available remote

Bioavailability of aspirin in rats comparing the drug's uptake into gastrointestinal tissue and vascular and lymphatic systems: implications on aspirin's chemopreventive action

84%
Lichtenberger L. M., Phan T., Fang D., Edler S., Philip J., Li-Geng T., Dial E. J.
Journal of Physiology and Pharmacology
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2016
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tom 67
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nr 5
11
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Ascorbic acid attenuates aspirin-induced gastric damage: role of inducible nitric oxide synthase

84%
Konturek P. C., Kania J., Hahn E. G., Konturek J. W.
Journal of Physiology and Pharmacology. Supplement
|
2006
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tom 57
|
nr 5
125-136
Aspirin (ASA) represents an important risk factor for gastric mucosal injury. Recently, vitamin C releasing aspirin (ASA-VitC) has been shown to reduce gastric toxicity of ASA in animal model of gastric injury. The aim of the present study was to compare the effect of ASA and ASA-VitC on the gastric mucosal damage before and after Helicobacter pylori (Hp) eradication in 10 young healthy Hp-positive volunteers. All subjects underwent endoscopy at day 0 (before ASA or ASA-VitC treatment) and at day 3 following treatment (1.6 g ASA/day or 1.6 g ASA + 0.96 g Vit C/day). In addition, in vitro experiments were performed in which gastric mucosal cell line (MKN-45 cells) was incubated with ASA or ASA-VitC alone or in combination with H.pylori. Expression of constitutive and inducible NO synthase (cNOS, iNOS) was analyzed by Western blot. Moreover, COX-2 expression was analyzed in gastric biopsies at mRNA and protein level by RT-PCR and Western blot, repectively. In humans, treatment with ASA-VitC induced significantly less gastric mucosal lesions than plain ASA. Furthermore, in comparision to plain ASA, ASA-VitC caused stronger inhibition of cNOS and increase in iNOS expression in the gastric mucosa. in vitro studies demonstrated a significant increase in iNOS expression in MKN-45 cells incubated with Hp. This effect was aggravated by the addition of ASA, but not ASA-VitC, to MKN-45 cells incubated with H.pylori. Both ASA and ASA-VitC stimulated the COX-2 expression in the gastric mucosa. We conclude that ASA-VitC in comparison with ASA induces less gastric mucosal damage and this protective effect may be due to its inhibitory effect on iNOS expression.
12
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Antithrombotic medications and their impact on fibrin clot structure and function

84%
Undas A., Zabczyk M.
Journal of Physiology and Pharmacology
|
2018
|
tom 69
|
nr 4
13
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NO-releasing aspirin exerts stronger growth inhibitory effect on Barrett's adenocarcinoma cells than traditional aspirin

84%
Konturek P. C., Kania J., Burnat G., Hahn E. G.
Journal of Physiology and Pharmacology. Supplement
|
2006
|
tom 57
|
nr 12
15-24
Expression of cyclooxygenase-2 (COX-2) is involved in the chronic inflammation-related development of Barrett’s adenocarcinoma and the use of selective COX-2 inhibitors (coxibs) might provide new chemoprevention strategy for Barrett’s adenocarcinoma (BA). Despite an excellent gastrointestinal (GI) safety profile of coxibs, their use is limited because of the possible cardiovascular complications. The coupling of NSAIDs with a NO-donating moiety has led to the birth of a new class of anti-inflammatory drugs, called the COX-inhibiting nitric oxide donators (CINODs). The member of this group, NO-aspirin (NO-ASA) retains the anti-inflammatory properties of traditional aspirin (ASA), but the release of NO accounts for anti-thromboembolic effect and better GI safety profile. The role of NO-ASA in the prevention of Barrett’s adenocarcinoma (BA) has not been studied so far. Therefore, the aim of the present study was: 1) to analyse the expression of COX-2 in the biopsies obtained from BE; 2) to compare the effect of NO-ASA with that of ASA on proliferation rate in Barrett’s adenocarcinoma cell line (OE-33 cells); 3) to determine the effect of both compounds on the apoptosis rate using FACS analysis and expression of 32-kDa procaspase-3 and active proapoptotic 20-kDa caspase-3 in OE-33 cell line. The expression of COX-2 was assessed in biopsies obtained from the Barrett’s mucosa and normal squamous epithelial esophageal mucosa from 20 BE patients by RT-PCR and Western blot analysis, respectively. The BA cell line (OE-33) was incubated with NO-ASA or ASA (10-1000µM). The cell proliferation and apoptosis rate was measured by BrdU and FACS-analysis, respectively. The expression of caspase-3 (active and inactive form) was analyzed by Western blot. In Barrett’s mucosa a significant up-regulation of COX-2 was observed. Compared with traditional ASA, NO-ASA caused a significantly stronger induction of apoptosis (dose-dependently). Inhibition of cell proliferation in OE-33 cells observed under NO-ASA treatment was due to the apoptosis induction. The increase in apoptotic rate was accompanied by the upregulation of active 20-kDa caspase-3. At the highest concentration (1000µM), a necrotic death of OE-33 cells was observed under NO-ASA treatment. We conclude that: NO-ASA caused induction of apoptosis in BA cell line and slight growth inhibition. These results indicate that this compound may represent a promising chemopreventive agent for Barrett’s adenocarcinoma.
14
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Thrombinogenesis and its pharmacological modulation in atherosclerosis

84%
Szczeklik A., Musial J., Dropinski J., Krzanowski M., Krolikowski W., Undas A., Swadzba J., Duplaga M., Bodzon W.
Journal of Physiology and Pharmacology
|
1994
|
tom 45
|
nr 1
15
Content available remote

Effect of aspirin on cysteinyl leukotrienes production by eosinophils co-cultured with epithelial cells

84%
Jawien J., Olszanecki R., Lorkowska B., Korbut R.
Journal of Physiology and Pharmacology
|
2004
|
tom 55
|
nr 4
Eosinophils have long been considered to play solely crucial role in the pathogenesis of aspirin-induced asthma, however increasing evidence suggest that the bronchial epithelium is also involved in the initiation and maintenance of allergic inflammation. Epithelial cells and eosinophils retained within airways interact reciprocally to mount and sustain inflammatory response. Recently, we have shown that eosinophil-epithelial cell interactions are capable of amplifying the production of cysteinyl leukotrienes (Cys-LTs). The aim of this study was to investigate if there is any influence of aspirin (ASA) on Cys-LTs and prostaglandin E2 (PGE2) production in the model of co-cultured human epithelial cells (line BEAS-2B) and human eosinophils. Synthesis of Cys-LTs in eosinophils was increased after incubation with ASA. At the same time the production of PGE2 was decreased by aspirin (n=32). BEAS-2B cells barely formed Cys-LTs; addition of ASA increased this production, while production of PGE2 was inhibited by aspirin (n=32). Synthesis of Cys-LTs by eosinophils co-incubated with BEAS-2B was nearly 7-fold higher than that of activated eosinophils alone (1631.5 pg/ml ± 154 vs. 258 pg/ml ± 31; p<0.05; n=32). Surprisingly, in the eosinophil-epithelial cell co-culture, aspirin inhibited both augmentation of Cys-LTs synthesis (from 1631.5 pg/ml ± 154 to 1458 pg/ml ± 137; p<0.05; n=32) and the production of PGE2 (from 2640 pg/ml ± 231 to 319 pg/ml ± 27; p<0.05; n=32). In summary, we have demonstrated that interactions between non-atopic eosinophils and epithelial cells result in augmentation of Cys-LTs production, and this augmentation could be inhibited by aspirin.
16
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Endothelial secretogogues and deformability of erythrocytes

84%
Korbut R. A., Adamek-Guzik T., Madej J., Korbut R.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 4,1
Many diseases of the heart and circulatory system have been linked with both dysfunction of vascular endothelium and insufficient deformability of erythrocytes. Using shear stress laser diffractometry we investigated whether deformability of erythrocytes would be regulated endogenously by generation of two endothelial secretogogues: prostacyclin and nitric oxide. Experiments were performed in rats ex vivo and with whole blood or isolated erythrocytes in vitro. Iloprost - a stable analogue of prostacyclin (10 µg/kg i.v.) and SIN-1 (NO-donor) at a dose of 2 mg/kg/min i.v induced a significant improvement of deformability of erythrocytes ex vivo. Improvements of deformability by these two compounds were also evident in vitro when they were applied at a range of concentrations of 1 µM and 3 µM, respectively. Cyclooxygenase (indomethacin 20 mg.kg i.v.) and nitric oxide synthase (L-NAME 10 mg/kg i.v.) inhibitors while worsening deformability ex vivo, they did not affect (3 mM and 10 µM, respectively) rheological functions of erythocytes in vitro. Aggravating effects of these inhibitors on erythrocyte deformability ex vivo were reversed by prostacyclin and nitric oxide supplemented exogenously. Aspirin at a low (1 mg/kg i.v.) and high dose (50 mg/kg i.v.), contrary to indomethacin and L- NAME, aggravated erythrocyte deformability either ex vivo or in vitro. It is concluded that autocrine function of vascular endothelium plays an important role in regulation of rheology of red blood cells in flowing blood. The mechanism of this phenomenon is unclear but some possible explanations are discussed. In addition, in our experiments aspirin revealed unique erythrocyte damaging properties, possibly independent of inhibition of cyclooxygenase, but related to a direct protein acetylation.
17
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Enhanced expression of leptin following acute gastric injury in rat

84%
Konturek P. C., Brzozowski T., Sulekova Z., Meixner H., Hahn E. G., Konturek S. J.
Journal of Physiology and Pharmacology
|
1999
|
tom 50
|
nr 4
18
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The role of capsaicin - sensitive sensory neurons and nitric oxide in regulation of gastric mucosal growth

84%
Dembinski A., Warzecha Z., Ceranowicz P., Konturek S. J.
Journal of Physiology and Pharmacology
|
1995
|
tom 46
|
nr 3
19
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Content available

The fight against rheumatism: from willow bark to COX-1 sparing drugs

84%
Vane J. R.
Journal of Physiology and Pharmacology
|
2000
|
tom 51
|
nr 4,1
20
Content available remote

The role of reactive oxygen species and capsaicin-sensitive sensory nerves in the pathomechanisms of gastric ulcers induced by stress

84%
Kwiecien S., Brzozowski T., Konturek P. C., Pawlik M. W., Pawlik W. W., Kwiecien N., Konturek S. J.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 3
Gastric microcirculation plays an important role in the maintenance of the gastric mucosal barrier and mucosal integrity. Sensory nerves are involved in the regulation of mucosal blood circulation and mucosal defense. Therefore, the ablation of these nerves by neurotoxic doses of capsaicin provides the possibility of determination of their role in gastric mucosal integrity. Stress ulceration represents a serious gastric lesions. Results of our previous experiments have indicated that water immersion and restraint stress (WRS) led to increased oxidative metabolism. Ablation of sensory nerves by high doses of capsaicin retards healing of gastric ulcers, but the role of reactive oxygen species (ROS) in the healing process has been little studied. Therefore, the aim of our present investigations was to determine the participation of ROS in sensory nerve activity during WRS. Experiments were caried out on 90 male Wistar rats and the area of gastric lesions was measured by planimetry.Colorimetric assays were used to determine gastric mucosal levels of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), as well as superoxide dismutase (SOD) activity. We demonstrated that inactivation of sensory nerves resulted in magnification of gastric mucosal damage induced by the WRS. In this process, oxidative stress, as reflected by an increase of MDA and 4-HNE tissue concentrations (an index of lipid peroxidation), as well as decrease of SOD activity, could play an important role. Aspirin, applied in a low dose, exerts a protective activity, possibly due to its metabolites, which possess the anti-oxidant and ROS scavanging properties. Pentoxyfilline-induced gastroprotection and hyperemia depends upon attenuation of the oxidative stress. This protection and hyperemia were, at least in part, attenuated by ASA.
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