Wyniki wyszukiwania

1

Golgi alpha-mannosidase II mediates the formation of vascular smooth muscle foam cells under inflammatory stress

100%

Zha K., Ye Q.

Folia Histochemica et Cytobiologica

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2021

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tom 59

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nr 2

2

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

72%

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.

3

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

58%

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.

4

Mouse models of experimental atherosclerosis

58%

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.

Ograniczanie wyników

3 Journal of Physiology and Pharmacology

1 Folia Histochemica et Cytobiologica

3 Jawien J.

3 Korbut R.

2 Gajda M.

2 Olszanecki R.

1 Nastalek P.

1 Wolkow P.

1 Ye Q.

1 Zha K.

1 Zuranska J.

1 2021

1 2008

1 2007

1 2004

Golgi alpha-mannosidase II mediates the formation of vascular smooth muscle foam cells under inflammatory stress

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

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

Mouse models of experimental atherosclerosis