Wyniki wyszukiwania - Biblioteka Nauki

1

Mouse models of experimental atherosclerosis

100%

Jawien J. , Nastalek P. , Korbut R.

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tom 55

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nr 3

EN

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.

2

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

88%

Pyka-Fosciak G. , Jawien J. , Gajda M. , Jasek E. , Litwin J. A.

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tom 64

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nr 6

3

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

76%

Jawien J. , Gajda M. , Wolkow P. , Zuranska J. , Olszanecki R. , Korbut R.

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nr 3

633-639

EN

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.

4

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

63%

Toton-Zuranska J. , Gajda M. , Pyka-Fosciak G. , Kus K. , Pawlowska M. , Niepsuj A. , Wolkow P. , Olszanecki R. , Jawien J. , Korbut R.

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nr 2

EN

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.

5

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

63%

Stefan J. , Kus K. , Wisniewska A. , Kaminski K. , Szczubialka K. , Jawien J. , Nowakowska M. , Korbut R.

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nr 5

6

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

63%

Maga P. , Sanak M. , Jawien J. , Rewerska B. , Maga M. , Wachsmann A. , Koziej M. , Gregorczyk-Maga I. , Nizankowski R.

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nr 3

7

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

63%

Jawien J. , Gajda M. , Mateuszuk L. , Olszanecki R. , Jakubowski A. , Szlachcic A. , Karabiowska M. , Korbut R.

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nr 3

EN

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.