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Antiplatelet action of losartan involves TXA2 receptor antagonism but not TXA2 synthase inhibition

100%

Chlopicki S., Koda M., Chabielska E., Buczko W., Gryglewski R. J.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 4,1

2

Reactivity of chicken chorioallantoic arteries, avian homologue of human fetoplacental arteries

84%

Lindgren I., Zoer B., Altimiras J., Villamor E.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 5

3

Differential effects of nitric oxide deficiency on primary tumour growth, pulmonary metastasis and prostacyclin/thromboxane A2 balance in orthotopic and intravenous murine models of 4T1 breast cancer

84%

Kij A., Kus K., Smeda M., Zakrzewska A., Proniewski B., Matyjaszczyk K., Jasztal A., Stojak M., Walczak M., Chlopicki S.

Journal of Physiology and Pharmacology

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2018

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tom 69

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nr 6

4

Prostaglandin E2 (PGE2) and thromboxane A2 (TXA2) synthesis is regulated by conjugated linoleic acids (CLA) in human macrophages

84%

Stachowska E., Dolegowska B., Dziedziejko V., Rybicka M., Kaczmarczyk M., Bober J., Rac M., Machalinski B., Chlubek D.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 1

77-85

Conjugated linoleic acid (CLAs) are positional and geometric isomers of linoleic acid with have a potential anti-atherosclerotic and anti-inflammation properties. Metabolites of arachidonic acid - prostaglandins and thromboxans are endogenous mediators of inflammation. Prostaglandin E2 and thromboxan A2 which are a products of two izoformes of cyclooxygenases (COX-1 and COX-2) in macrophages, play an important role in this process. COX - 1 is a constitutive enzyme, whereas the COX - 2 is inducible and its amount in the cell rapidly increases during inflammation (e.g. via NF B pathway). The aim of the study was to test the effect of CLAs on cyclooxygenases (COX-1 and COX-2) activity, their mRNA expression and protein content in macrophages. Additionally the active form of the kB (NF B) transcription factor was measured. For the experiments monocytes from monocytic cell line (THP-1) and from human venous blood were used. Monocytes were differentiated to macrophages and cultured with 30 µM CLAs or linoleic acid for 48 h. The COX-1 and COX-2 products - PGE2 and TXB2, were measured by ELISA method. The enzymes (COX-s) activity were estimated by spectroscopic method. mRNA expression and protein analysis were analysed by real-time PCR and Western blot technique. In macrophages cultured with CLAs reduction of TXB2 and PGE2 concentration was observed. Significant change in COX-2 expression in cells cultured with trans-10, cis-12 CLA (in macrophages obtained from peripheral blood) was observed. COX-1 inhibition was resulting from competition of CLA and linoleic acid with arachidonic acid.

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The role of cyclooxygenase [COX]-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration

84%

Pecanha F. M., Wiggers G. A., Briones A. M., Perez-Giron J. V., Miguel M., Garcia-Redondo A. B., Vassallo D. V., Alonso M. J., Salaices M.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 1

29-36

We have previously demonstrated that chronic exposure to low-dose of mercury induced endothelial dysfunction and increased vasoconstrictor responses. The aim of this work was to investigate if mercury exposure alters contractile prostanoids production from cyclooxygenase-2 (COX-2) and its contribution to phenylephrine responses. For this, aortic segments from 3-month old Wistar rats daily treated with HgCl2 (1st dose 4.6 µg/kg, subsequent dose 0.07 µg/kg/day, i.m.) or vehicle for 30 days were used. Mercury treatment did not affect systolic blood pressure but increased phenylephrine-induced vasoconstriction. The non selective COX inhibitor, indomethacin (10 µmol/l) reduced the response to phenylephrine more in aortic segments from mercury-treated than control rats. The selective COX-2 inhibitor NS 398 (1 µmol/l), the thromboxane A2/prostaglandin H2 receptor (TP) antagonist SQ 29,548 (1 µmol/l), the TXA2 synthase inhibitor furegrelate (1 µmol/l), the EP1 receptor antagonist SC 19220 (1 µmol/l) and the AT1 receptor antagonist losartan (10 µmol/l) reduced phenylephrine response only in vessels from mercury-treated rats. TXA2 and PGE2 levels were greater in the incubation medium of vessels from treated than untreated rats; NS 398 decreased these levels only in the mercury group. COX-2 protein was localized in adventitial and endothelial cells. Aortic COX-2 mRNA expression and plasma angiotensin converting enzyme activity were greater in mercury-treated rats. These results suggest that treatment with low doses of mercury increases the release of COX-2-derived vasoconstrictor prostanoids and its participation in phenylephrine responses. The increased activation of the renin-angiotensin system after mercury treatment might be associated to this increased COX-2 activity.

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Increased aortic atherosclerotic plaque development in female apolipoprotein E-null mice is associated with elevated thromboxane A2 and decreased prostacyclin production

67%

Smith D. D., Tan X., Tawfik O., Milne G., Stechschulte D. J., Dileepan K. N.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 3

309-316

The production of thromboxane A2 (TXA2) and prostacyclin (prostaglandin I2, PGI2) is known to be increased in patients with atherosclerosis. In this study, we evaluated the influence of gender on TXA2 and PGI2 production, and their association with the progression of atherosclerosis in apolipoprotein E-null (ApoE-/-) mice maintained on a high fat diet for 3 months. En face analyses of aortas showed marked increases in plaque formation in female ApoE-/- mice. Quantification of the hematoxylin/eosin (H&E) stained cross sections of the aortic arch revealed 3 to 4-fold higher plaque thickness in female ApoE-/- mice. Analyses of 24-hours urine samples for 11-dehydro TXB2 and 2, 3-dinor-6-keto PGF1alpha indicated that female ApoE-/- mice produce up to 15-fold more TXA2 and 50% less PGI2 than the age matched males. Interestingly, the serum cholesterol levels in ApoE-/- females were 20% lower than males on the high fat regimen. No gender-associated changes in the number of T lymphocytes, mast cells and macrophages were evident in the lesion areas of ApoE-/- mice. The results suggest that the markedly elevated TXA2 production and reduced PGI2 production are gender-related proatherogenic risk factors in female ApoE-/- mice.

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Role of thromboxane A2 and platelet activating factor in early haemodynamic response to lipopolysaccharide in rats

67%

Bochenski J., Chlopicki S., Gryglewski R. J.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 2

8

Expression of cyclooxygenase-1 and cyclooxygenase-2 in normal and pathological human oral mucosa

59%

Mauro A., Lipari L., Leone A., Tortorici S., Burruano F., Provenzano S., Gerbino A., Buscemi M.

Folia Histochemica et Cytobiologica

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2010

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tom 48

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nr 4

Ograniczanie wyników

Antiplatelet action of losartan involves TXA2 receptor antagonism but not TXA2 synthase inhibition

Reactivity of chicken chorioallantoic arteries, avian homologue of human fetoplacental arteries

Differential effects of nitric oxide deficiency on primary tumour growth, pulmonary metastasis and prostacyclin/thromboxane A2 balance in orthotopic and intravenous murine models of 4T1 breast cancer

Prostaglandin E2 (PGE2) and thromboxane A2 (TXA2) synthesis is regulated by conjugated linoleic acids (CLA) in human macrophages

The role of cyclooxygenase [COX]-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration

Increased aortic atherosclerotic plaque development in female apolipoprotein E-null mice is associated with elevated thromboxane A2 and decreased prostacyclin production

Role of thromboxane A2 and platelet activating factor in early haemodynamic response to lipopolysaccharide in rats

Expression of cyclooxygenase-1 and cyclooxygenase-2 in normal and pathological human oral mucosa