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1
Content available remote

The current view on the role of leukotrienes in atherogenesis

100%
Jawien J., Korbut R.
Journal of Physiology and Pharmacology
|
2010
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tom 61
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nr 6
2
Content available remote

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

81%
Jawien J., Olszanecki R., Lorkowska B., Korbut R.
Journal of Physiology and Pharmacology
|
2004
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tom 55
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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.
3
Content available remote

Bay x 1005 attenuates atherosclerosis in apoE-LDLR - double knockout mice

81%
Jawien J., Gajda M., Olszanecki R., Korbut R.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 3
Recently, we have shown that MK-886 - an inhibitor of five lipoxygenase activating protein (FLAP) inhibits atherosclerosis in apolipoprotein E / LDL receptor - double knockout mice. We, therefore, wanted to find out if other FLAP inhibitor - BAYx1005 given at a dose of 1.88 mg per 100 mg of body weight per day during 16 weeks, could also attenuate atherogenesis. In apoE/LDLR - DKO mouse model BAYx1005 inhibited atherogenesis, measured both by "en face" method (23.84 ± 2.7% vs. 15.16 ± 1.4%) and "cross-section" method (497236 ± 31516 µm2 vs. 278107 ± 21824 µm2). This is the first report that shows the effect of BAYx1005 on atherogenesis in gene-targeted mice.
4
Content available remote

The involvement of adhesion molecules and lipid mediators in the adhesion of human platelets to eosinophils

81%
Jawien J., Lomnicka M., Korbut R., Chlopicki S.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 4
Platelet-leukocyte interactions represent an important determinant of the inflammatory response. Although mechanisms of platelet-neutrophil adhesion were studied extensively, little is known on the mechanisms of platelet-eosinophil interactions. The aim of the present study was to analyze the involvement of adhesion molecules and lipid mediators in platelet-eosinophil adhesion as compared to platelet-neutrophil adhesion. For that purpose human platelets, eosinophils and neutrophils were isolated and platelet-eosinophil and platelet-neutrophil adhesion induced by thrombin (30 mU/ml), LPS (0.01 µg/ml) and fMLP (1 µM) was quantified using the "rosettes" assay. The involvement of adhesion molecules such as selectin P, glycoprotein IIb/IIIa (GPIIb/IIIa) and lipid mediators such as of thromboxane A2 (TXA2), platelet activating factor (PAF) and cysteinyl leukotrienes (cysLTs) were studied using monoclonal antibodies and pharmacological inhibitors, respectively. Thrombin (30 mU/ml), LPS (0.01 µg/ml) and fMLP (1 µM) each of them induced platelet-eosinophil adhesion that was even more pronounced as compared with platelet-neutrophil adhesion induced by the same stimulus. Anti-CD62P antibody (1 µg/ml) and anti-GP IIb/IIIa antibody (abciximab - 3 µg/ml) strongly inhibited platelet-eosinophil as well as platelet-neutrophil adhesion. Aspirin inhibited platelet-eosinophil adhesion, while MK 886 - a FLAP inhibitor (10 µM), or WEB 2170 - a PAF receptor antagonist (100 µM) were less active. On the other hand aspirin, MK 886 and WEB 2170 all three of them inhibited platelet-neutrophil adhesion. In summary, platelets adhered avidly to eosinophils both after activation of platelets by thrombin, eosinophils by fMLP or simultaneous activation of platelets and eosinophils by LPS. Similarly to platelet-neutrophil interaction adhesion of platelets to eosinophils involved not only adhesion molecules (selectin P, GPIIb/IIIa), but also lipid mediators such as TXA2. The involvement of PAF and cysteinyl leukotrienes in platelet-eosinophil adhesion was less pronounced as compared to platelet-neutrophil adhesion.
5
Content available remote

Mouse models of experimental atherosclerosis

81%
Jawien J., Nastalek P., Korbut R.
Journal of Physiology and Pharmacology
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2004
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tom 55
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nr 3
Since 1992 the mouse has become an excellent model for experimental atherosclerosis research. Until 1992, the diet - induced atherosclerosis mouse model has been used effectively, but the lesions tended to be small and were limited to early fatty-streak stage. This model was also criticized because of the toxicity and inflammatory responses due to the diet. In 1992 the first line of gene targeted animal models, namely apolipoprotein E - knockout mice was developed. Of the genetically engineered models, the apoE - deficient model is the only one that develops extensive atherosclerotic lesions on a chow diet. It is also the model in which the lesions have been characterized most thoroughly. The lesions develop into fibrous plaques; however, there is no evidence that plaque rupture occurs in this model. The LDL receptor - deficient model has elevated LDL levels, but no lesions, or only very small lesions, form on the chow diet, however, robust lesions do form on the western-type diet. The creation of apoE - knockout mice has changed the face of atherosclerosis research.
6
Content available remote

Effect of nebivolol treatment on atherosclerotic plaque components in apoE-knockout mice

71%
Pyka-Fosciak G., Jawien J., Gajda M., Jasek E., Litwin J. A.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 6
7
Content available remote

Eosinophil - epithelial cell interaction augments cysteinyl leukotrienes synthesis

71%
Jawien J., Chlopicki S., Olszanecki R., Lorkowska B., Gryglewski R. J.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 1
Eosinophils accumulation in the airways and sustained eosinophil-derived cysteinyl leukotrienes production represent key elements of the inflammatory response seen in asthma.However,it is not known whether activated epithelial cells influence cysteinyl leukotrienes production by eosinophils from healthy valunteers.The aim of the present study was therefore to analyse the effects of interactions between non-atopic eosinophils and epithelial cells on cysteinyl leukotrienes production in vitro .We measured cysteinyl leukotrienes released by phorbol 12-myristate 13-acetate (PMA)–activated human eosinophils or epithelial cells (human bronchial epithelial cell line -BEAS-2B)cultured alone or together.While activated BEAS-2B cells barely formed leukotrienes (1.39 pg/ml ± 0.2))(n=32),activated eosinophils produced considerable amount of them (62.25 pg/ml ± 10.29))(n=32).Interestingly,when activated eosinophils and epithelial cells were co-incubated,production of cysteinyl leukotrienes increased substantially (571.1 pg/ml ± 80.9))(n=32).Thus,eosinophil-epithelial cell interactions,when occur,are associated with increased biosythesis of cysteinyl leukotrienes.
8
Content available remote

Inhibition of NOS-2 induction in LPS-stimulated J774.2 cells by 1,5-isoquinolinediol, an inhibitor of PARP

71%
Olszanecki R., Gebska A., Jawien J., Jakubowski A., Korbut R.
Journal of Physiology and Pharmacology
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2006
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tom 57
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nr 1
Activation of both poly (ADP-ribose) polymerase (PARP) and inducible nitric oxide synthase (NOS-2) have been implicated in the pathogenesis of various forms of inflammation, therefore compounds which may simultaneously inhibit both pathways are of potential therapeutic interest. We tested the influence of potent inhibitor of PARP, 1, 5-isoquinolinediol (ISO), on NOS-2 induction in model of mouse macrophages (cell line J774.2) stimulated with lipopolysaccharide (1 µg/ml). Pretreatment with ISO (1-300 µM) resulted in dose-dependent inhibition of accumulation of NOS-2-derived nitrite in culture medium (IC50 = 9,3 µM) as well as inhibition of NOS-2 protein induction in cultured J774.2 cells; ISO given 10 hours after LPS did not influence activity of NOS-2. Interestingly, another PARP inhibitor, 3-aminobenzamide (3-AB, 10-3000 µM), did not influence 24-hr nitrite accumulation in J774.2 cell culture, either administered 15 minutes prior to LPS or 10 hrs after LPS. Scavenging of reactive oxygen species by use of mixture of SOD and catalase (SOD/Cat, 100/300 - 1000/3000 U/ml) as well as cell permeable SOD-mimetic [Mn(III)TBAP, 1- 100 µM], did not influence NOS-2 induction in J774.2 cells. In summary, we identified 1, 5-isoquinoline as potent inhibitor of induction of NOS-2 in LPS-treated mouse macrophages. The exact mechanism of inhibitory action of this compound on NOS-2 induction requires further investigation.
9

Triple immunofluorescence labeling of atherosclerotic plaque components in apoE-LDLR mice

61%
Gajda M., Jawien J., Mateuszuk L., Lis G. J., Radziszewski A., Chlopicki S., Litwin J. A.
Folia Histochemica et Cytobiologica
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2008
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tom 46
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nr 2
143-146
10
Content available remote

Significant deterioration of anti-atherogenic efficacy of nebivolol in a double (apolipoprotein E and endothelial nitric oxide synthase) knockout mouse model of atherosclerosis in comparison to single (apolipoprotein E) knockout model

61%
Kus K., Wisniewska A., Toton-Zuranska J., Olszanecki R., Jawien J., Korbut R.
Journal of Physiology and Pharmacology
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2014
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tom 65
|
nr 6
11
Content available remote

The effect of montelukast on atherogenesis in APOE-LDLR-double knockout mice

61%
Jawien J., Gajda M., Wolkow P., Zuranska J., Olszanecki R., Korbut R.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 3
633-639
We have shown that inhibitors of five lipoxygenase activating protein (FLAP) - MK-886 and BAYx1005 inhibit atherosclerosis in apolipoprotein E / LDL receptor - double knockout mice. We, therefore, investigated whether cysteinyl leukotrienes receptor inhibitor - montelukast, given at a dose of 0.125 µg per 100 mg of body weight per day during 16 weeks, could also attenuate atherogenesis. In apoE/LDLR - DKO mouse model montelukast significantly decreased atherogenesis, measured both by "en face" method (25.5±2.% vs. 17.23 ± 1.8%) and "cross-section" method (455 494 ± 26 477 µm2 vs. 299 201 ± 20 373 µm2). The results were, however, less pronounced, comparing to FLAP inhibitors. This is the first report showing the effect of montelukast on atherogenesis in gene-targeted mice.
12
Content available remote

Kaempferol, but not resveratrol inhibits angiotensin converting enzyme

61%
Olszanecki R., Bujak-Gizycka B., Madej J., Suski M., Wolkow P. P., Jawien J., Korbut R.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 2
Inhibition of angiotensin converting enzyme (ACE) has proved to be beneficial in the treatment of various cardiovascular disorders. The aim of this study was to evaluate ACE inhibitory potential of two polyphenolic compounds with different structures: resveratrol (present in high quantities in French wine) and kaempferol (abundant in greens), using method of liquid chromatography coupled with electrospray ionization mass spectrometry (LC-ESI-MS) for ex vivo measurement of angiotensin I to angiotensin II conversion by ACE in aortic tissue of Wistar-Kyoto rats. In this setting, kaempferol (10-30-100 µM), but not resveratrol (10-30-100 µM) appeared to inhibit dose-dependently conversion of Ang I to Ang II. Although the mechanism of ACE inhibition by kaempferol remains to be elucidated, this observation may help in search or designing of new classes of ACE inhibitors.
13
Content available remote

AVE 0991 - angiotensin-(1-7) receptor agonist, inhibits atherogenesis in apoE - knockout mice

51%
Toton-Zuranska J., Gajda M., Pyka-Fosciak G., Kus K., Pawlowska M., Niepsuj A., Wolkow P., Olszanecki R., Jawien J., Korbut R.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 2
Recent evidence shows that the renin-angiotensin system is a crucial player in atherosclerotic processes. It was also proved that Ang II promotes atherogenesis. Angiotensin-(1-7) [Ang-(1-7)] opposites Ang II action. Therefore, we would like to find out whether Ang-(1-7) receptor agonist: AVE 0991, could ameliorate atherosclerosis progression in an experimental model of atherosclerosis: apolipoprotein E (apoE) - knockout mice. AVE 0991 inhibited atherogenesis, measured both by “en face” method (7.63±1.6% vs. 14.6±2.1%) and “cross-section” method (47 235±7 546 µm2 vs. 91 416±8 357 µm2). This is the first report showing the effect of AVE 0991 on atherogenesis in gene-targeted mice.
14
Content available remote

Angiotensin 1-7 formation in breast tissue is attenuated in breast cancer - a study on the metabolism of angiotensinogen in breast cancer cell lines

51%
Bujak-Gizycka B., Madej J., Bystrowska B., Toton-Zuranska J., Kus K., Kolton-Wroz M., Jawien J., Olszanecki R.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 4
15
Content available remote

11-Dehydro thromboxane B2 levels after percutaneous transluminal angioplasty in patients with peripheral arterial occlusive disease during a one year follow-up period

51%
Maga P., Sanak M., Jawien J., Rewerska B., Maga M., Wachsmann A., Koziej M., Gregorczyk-Maga I., Nizankowski R.
Journal of Physiology and Pharmacology
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2016
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tom 67
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nr 3
16
Content available remote

The influence of angiotensin-(1-7) peptidomimetic (AVE 0991) and nebivolol on angiotensin i metabolism in aorta of apoE-knockout mice

51%
Olszanecki R., Suski M., Gebska A., Toton-Zuranska J., Kus K., Madej J., Bujak-Gizycka B., Jawien J., Korbut R.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 3
17
Content available remote

New cationically modified pullulan attenuates atherogenesis and influences lipid metabolism in apoE-knockout mice

51%
Stefan J., Kus K., Wisniewska A., Kaminski K., Szczubialka K., Jawien J., Nowakowska M., Korbut R.
Journal of Physiology and Pharmacology
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2016
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tom 67
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nr 5
18
Content available remote

Effect of curcumin on atherosclerosis in apoE-LDLR - double knockout mice

51%
Olszanecki R., Jawien J., Gajda M., Mateuszuk L., Gebska A., Korabiowska M., Chlopicki S., Korbut R.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 4
It is widely appreciated that inflammation and oxidant stress contribute to atherogenesis. Curcumin, a polyphenolic natural compound has been reported to possess anti-inflammatory and anti-oxidant actions. We hypothesized that curcumin could inhibit the development of atherosclerosis in the apoE/LDLR - double knockout mice fed with Western diet (21% fat, 0.15% cholesterol w/w, without cholic acid). Curcumin (purity 98%), premixed with diet, was given for 4 months at a dose of 0.3 mg/per day/per mouse. In this model curcumin inhibited atherogenesis, measured both by "en face" method (25,15±2,9% vs. 19,2±0,6%, p<0,05) and "cross-section" method (565867±39764 µm2 vs. 299201±20373 µm2, p<0,05). Importantly, curcumin influenced neither the concentrations of cholesterol and triglycerides in blood nor animal body weight. To our knowledge, this is the first report that shows the anti-atherogenic effect of low dose of curcumin in fine model of atherosclerosis: gene-targeted apoE/LDLR - double knockout mice.
19
Content available remote

Inhibition of nuclear factor-kappaB attenuates atherosclerosis in apoE-LDLR - double knockout mice

51%
Jawien J., Gajda M., Mateuszuk L., Olszanecki R., Jakubowski A., Szlachcic A., Karabiowska M., Korbut R.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 3
Nuclear factor - B (NF-B) is a good therapeutic target for cardiovascular disease and numerous efforts are being made to develop safe NF-B inhibitors. Nowadays many authors address NF-B as a major therapeutic target in atherosclerosis, especially for preventive measures, in the light of two main hypothesis of atherosclerosis: oxidation and inflammation. We hypothesized that ammonium pyrrolidinedithioocarbamate (PDTC) - a well-known inhibitor of NF-B could inhibit the development of atherosclerosis in this experimental model. We used apoE/LDLR - DKO mouse model, which is considered as a one of the best models to study the anti-atherosclerotic effect of drugs. In this model PDTC inhibited atherogenesis, measured both by "en face" method (25,15±2,9% vs. 15,63±0,6%) and "cross-section" method (565867±39764 µm2 vs. 291695±30384 µm2). Moreover, PDTC did not change the profile of cholesterol and triglycerides in blood. To our knowledge, this is the first report that shows the effect of PDTC on atherogenesis in gene-targeted apoE/LDLR - double knockout mice.
20
Content available remote

The effect of nebivolol on atherogenesis in apoE - knockout mice

42%
Kus K., Gajda M., Pyka-Fosciak G., Toton-Zuranska J., Pawlowska M., Suski M., Niepsuj A., Nowak B., Wolkow P., Olszanecki R., Jawien J., Korbut R.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 4
163-165
Nebivolol is a novel beta1-blocker with a nitric oxide (NO) - potentiating, vasodilatory effect that is unique among beta-blockers. It was already shown that nebivolol ameliorates atherosclerosis in cholesterol-fed rabbits. We, therefore, wanted to investigate whether this is the case in the fine experimental model of atherosclerosis: apolipoprotein E (apoE)- knockout mice. Nebivolol attenuated atherogenesis, measured both by "en face" method (9.23±1.8% vs. 14.6±2.1%) and "cross-section" method (63125±8455 µm2 vs. 91416±8357 m2). This is the first report showing the effect of nebivolol on atherogenesis in gene-targeted mice.
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