Wyniki wyszukiwania

1

Tubular and vascular actions of cytochrome P450-arachidonate metabolites

100%

Carrol M. A., Balazy M., McGiff J. C.

Journal of Physiology and Pharmacology. Supplement

|

1993

|

tom 44

|

nr 2

2

Involvement of arachidonic acid and its products in the mechanism of progesterone influence on its own production in vitro in bovine corpus luteum

88%

Kotwica J.

Bulletin of the Veterinary Institute in Puławy

|

2004

|

tom 48

|

nr 3

3

Nuclear import of arachidonate 5-lipoxygenase

75%

Brock T. G., Healy A. M.

Archivum Immunologiae et Therapiae Experimentalis

|

2000

|

tom 48

|

nr 6 Spec.Iss.

481-486

4

The effect of the type and amount of fat in diet on the composition of fatty acids in tissue lipids in experimental hypercholesterolaemia

75%

Ziemlanski S., Budzynska-Topolowska J., Rodkiewicz B.

Żywienie Człowieka i Metabolizm

|

1991

|

tom 18

|

nr 4

The efects were studied of the quality and amount of dietary fat on the pattern of fatty acids in the lipids of the serum and certain tissues (adipose fat, perirenal fat, liver, heart, testes) of guined pigs during experimentally induced hypercholesterolemia. During 12 weeks the animals received experimental diets containg 10% or 20% of energy from animal fats (butter, lard 2:3), sunflower oil or low-erucic rapeseed oil. Two control groups were chosen, receiving diets for animals without cholesterol or with 0.1% cholesterol added. The addition of cholesterol to the diet raised the content of the essential unsaturated fatty acids and polyunsaturated fatty acids in the adipose fat and hepatic lipids, and decreased their content in myocardial lipids. In testicular lipids changes were noted in the synthesis of long-chain polyunsaturated fatty acids. The addition of vegetable fats to the diet increased the content of linoleic acid in these tissues with a simultaneous decrease of arachidonic acid synthesis. It may be supposed that there is an upper range of arachidonic acid synthesis in the lipids of the studied tissues independent of dietary EFA and PUFA value.

5

Cytochrome P-450 metabolites in renal circulation and excretion - interaction with nitric oxide [NO] system

75%

Kompanowska-Jezierska E., Kuczeriszka M.

Journal of Physiology and Pharmacology. Supplement

|

2008

|

tom 59

|

nr 9

137-149

6

Regulation of the NADPH oxidase activity and anti-microbial function of neutrophils by arachidonic acid

75%

Hii C. S., Ferrante A.

Archivum Immunologiae et Therapiae Experimentalis

|

2007

|

tom 55

|

nr 2

7

The effect of packed red blood cell storage on arachidonic acid and advanced glycation end-product formation

75%

Lysenko L., Mierzchala M., Gamian A., Durek G., Kubler A., Kozlowski R., Sliwinski M.

Archivum Immunologiae et Therapiae Experimentalis

|

2006

|

tom 54

|

nr 5

8

Production of prostacyclin and prostaglandin E2 in resting and IL-1beta-stimulated A549, HUVEC and hybrid EA.HY 926 cells

75%

Olszanecki R., Gebska A., Korbut R.

Journal of Physiology and Pharmacology

|

2006

|

tom 57

|

nr 4

Production of arachidonic acid (AA) metabolites - prostacyclin (PGI2) in large vessels and prostaglandin E2 (PGE2) in microcirculation is intrinsically involved in maintenance of vascular wall homeostasis. EA.hy 926 is a hybrid cell line, is derived by fusion of HUVEC with A549 cells. The aim of this study was to examine the production of prostacyclin and PGE2 in resting and IL-1ß-stimulated EA.ha 926 cells, in comparison with its progenitor cells. Non-stimulated EA.hy 926 cells has been found to produce much lower amounts of prostacyclin than resting HUVEC. Resting hybrid cells produced more PGE2 than prostacyclin, despite they expressed high levels of COX-1 and PGI2 synthase. On the contrary to HUVEC and A549, EA.hy 926 cells did not respond to IL-1ß with COX-2 induction and increase of prostaglandin production, however they did it in response to lysophosphatidylcholine (LPC). The characteristics of EA.hy 926 cells in terms of the pattern of prostanoid formation could facilitate studies on endothelial metabolism and role of these important lipid mediators.

9

Modulation of NMDA receptor-mediated release of [3H]arachidonate in hippocampal slices of immature rats

75%

Salinska E., Lazarewicz J. W.

Acta Neurobiologiae Experimentalis

|

1995

|

tom 55

|

nr 1

10

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Functional aspects of eicosanoid metabolism

63%

Carroll M. A., McGiff J. C.

Journal of Physiology and Pharmacology

|

1991

|

tom 42

|

nr 3

The sequential metabolism of eicosanoids by AA oxygenases confers biological properties that may have significant functional implications. Further- the interpretation of the effects of cyclooxygenase inhibitors on eicosanoid, dependent mechanisms needs to be reevaluated. Previously, if cyclooxygenase inhibitors affected the biological action of AA, it was considered to be due to elimination of a prostanoid-mediated component. This interpretation is no longer valid if a cell or tissue has significant P450 and cyclooxygenase activity. The cellular proximity of the P450-dependent monooxygenases and cyclooxygenase, described in tubules, interstitial cells, and blood vessels, may confer a unique ability of A A metabolites to coordinate tubular and vascular function.

11

Cardioprotective effect of 5-lipoxygenase gene [ALOX5] silencing in ischemia-reperfusion

63%

Lisovyy O. O., Dosenko V. E., Nagibin V. S., Tumanovska L. V., Korol M. O., Surova O. V., Moibenko O. O.

Acta Biochimica Polonica

|

2009

|

tom 56

|

nr 4

687-694

It is well known that 5-lipoxygenase derivates of arachidonic acid play an important pathogenic role during myocardial infarction. Therefore, the gene encoding arachidonate 5-lipoxygenase (ALOX5) appears to be an attractive target for RNA interference (RNAi) application. In experiments on cultivated cardiomyocytes with anoxia-reoxygenation (AR) and in vivo using rat model of heart ischemia-reperfusion (IR) we determined influence of ALOX5 silencing on myocardial cell death. ALOX5 silencing was quantified using real-time PCR, semi-quantitative PCR, and evaluation of LTC4 concentration in cardiac tissue. A 4.7-fold decrease of ALOX5 expression (P < 0.05) was observed in isolated cardiomyocytes together with a reduced number of necrotic cardiomyocytes (P < 0.05), increased number live (P < 0.05) and unchanged number of apoptotic cells during AR of cardiomyocytes. Downregulation of ALOX5 expression in myocardial tissue by 19% (P < 0.05) resulted in a 3.8-fold reduction of infarct size in an open chest rat model of heart IR (P < 0.05). Thus, RNAi targeting of ALOX5 protects heart cells against IR injury both in culture and in vivo.

12

DNA methylation, induced by beta-carotene and arachidonic acid, plays a regulatory role in the pro-angiogenic VEGF-receptor (KDR) gene expression in endothelial cells

63%

Kiec-Wilk B., Razny U., Mathers J. C., Dembinska-Kiec A.

Journal of Physiology and Pharmacology

|

2009

|

tom 60

|

nr 4

49-53

DNA methylation is a potent regulator of gene expression. The influence of beta-carotene (BC) and arachidonic acid (AA) on angiogenesis - a new blood vessel formation, was reported. The tyrosine kinase VEGFR-2 receptor (KDR) activation by vascular endothelial growth factor is one of the main angiogenic mechanisms. This study was aimed to investigate a possible role of CpG island methylation on regulation of the pro-angiogenic KDR gene expression after incubation of human endothelial cells with BC and/or AA. Methods: Human umbilical vein endothelial cells (HUVEC) were incubated with BC (1-10 µM) and/or 3 µM AA for 24 hours. The CpG island methylation was quantified using the COBRA method and restriction enzymes' digestion (NewEngland BioLabs). Intracellular protein concentrations were determined by Western blot analysis using the specific antibodies (Santa Cruz). Results: Incubation with BC and AA, decreased methylation of the KDR promoter region. These results well-correlated with the detected, by qRT-PCR, up-regulation of KDR gene expression by BC (p=0.035) as well as by AA. Incubation with BC (p=0.02) and AA (p=0.0014) increased the KDR protein levels in HUVECs. Conclusion: The changes in CpG island methylation of the KDR the pro-angiogenic gene promoter, represents one of the mechanisms involved in regulation of angiogenic response by BC and AA.

13

Biosynthesis of prostaglandins in pathogenic and non-pathogenic strains of Acanthamoeba castellanii

63%

Hadas E.

Acta Protozoologica

|

1988

|

tom 27

|

nr 1

14

Functional analysis of eicosanoids from white blood cells in sepsis and SIRS

63%

Baenkler M., Leykauf M., John S.

Journal of Physiology and Pharmacology. Supplement

|

2006

|

tom 57

|

nr 12

25-33

Sepsis and SIRS are affections with major alterations in inflammatory activity. The impact of prostaglandins (PG) and leukotrienes (LT) produced from white blood cells (WBC) in this context is not completely understood. Thirty nine patients with sepsis or SIRS were investigated in comparison to 10 healthy controls. WBC were collected and separately exposed to arachidonic acid (AA) or to nothing else. After centrifugation, the generated PGE2 and LTCDE4 with or without stimulation were measured in the supernatant. LT-levels were significantly higher during sepsis/SIRS than in controls whereas PG-levels of patients were decreased to those of controls in basic condition. The relation between the level with and without stimulation showed a significant higher ratio in PG in contrast to LTs. The survivor’s ratio in LT levels was significantly higher than that of non-survivors, which did not differ from controls. Generation of LT from WBC is enhanced during sepsis/SIRS, but LT generation after stimulation only in survivors but not in non-survivors. This inability of WBC to generate LT during sepsis in non-survivors could be predictive regarding the outcome of sepsis/SIRS and may be part of the “immunoparalysis” seen during sepsis in association with bad outcome.

15

Topography and morphometry of intestinal mast cells in children with Hirschsprung's disease

63%

Hermanowicz A., Debek W., Dzienis-Koronkiewicz E., Chyczewski L.

Folia Histochemica et Cytobiologica

|

2008

|

tom 46

|

nr 1

65-68

16

Peroxisome proliferator-activated receptor alpha activation inducesunfavourable changes in fatty acid composition of myocardial phospholipids

63%

Baranowski M., Blachnio-Zabielska A., Gorski J.

Journal of Physiology and Pharmacology

|

2009

|

tom 60

|

nr 2

13-20

Peroxisome proliferator-activated receptor alpha (PPAR) plays a crucial role in the transcriptional regulation of myocardial lipid metabolism. In vitro studies on isolated cardiomyocytes showed that PPAR activation induces expression of numerous genes involved in virtually all steps of fatty acid catabolism. However, there is very few data on the effect of PPAR activation on the content and composition of myocardial lipids in vivo. Therefore, our main aim was to examine effects of selective PPAR agonist WY-14643 on the content and fatty acid composition of major lipid classes in the heart of rats fed a standard chow (STD) or a high-fat diet (HFD). In STD rats WY-14643 paradoxically decreased palmitate oxidation rate in the heart, however, in HFD animals such effect was not observed. WY-14643 markedly reduced myocardial free fatty acid and diacylglycerol content in STD rats, whereas in HFD group the opposite effect was observed. These changes reflected alterations in plasma lipid concentration which suggests that effects of WY-14643 on the heart were indirect and secondary to changes in plasma lipid availability induced by the drug. Basal myocardial glucose uptake was not affected by PPAR agonist in either group, however, glycogen content in the heart was markedly increased. WY-14643 exerted profound influence on the fatty acid composition of myocardial phospholipids in both diet groups. These changes included increased percentage of monounsaturated fatty acids and replacement of n-3 polyunsaturated fatty acids (PUFA) by those from the n-6 family. This action of WY-14643 might be detrimental to the heart since n-3 PUFA possess cardioprotective and antiarrhythmic properties.

17

Pharmacological inhibition of leukotriene biosynthesis: effects on the heart conductance

63%

Sanak M., Dropinski J., Sokolowska B., Faber J., Rzeszutko M., Szczeklik A.

Journal of Physiology and Pharmacology

|

2010

|

tom 61

|

nr 1

53-58

Leukotrienes are lipid mediators produced via 5-lipooxygenase pathway of arachidonic acid. At least two cysteinyl-leukotrienes receptors are highly expressed in the heart, including the conduction system. Coronary angiography or angioplasty is accompanied by release of cysteinyl leukotrienes into coronary circulation and into urine. We tested the hypothesis that inhibition of leukotrienes biosynthesis would affect the conductance system function. In a double-blind placebo controlled study, patients with stable angina undergoing elective coronary catheterization or angioplasty were randomly assigned to 48 hrs treatment with a 5-lipoxgenase inhibitor (n=54) or placebo (n=49). ECG Holter recording was carried out for 24 hrs before and after the procedure and urinary leukotriene E4 measurements were done. Inhibition of 5-lipoxygenase caused 26% reduction of urinary leukotriene E4, associated with: 1) decrease in heart rate by about 7%, 2) enhanced heart rate variability; 3) protection against depressions in atrioventricular conductance and ventricular repolarization induced by the procedure. No effects on either arrhythmias, or ECG patterns of ischemia were noted. We conclude that pharmacological inhibition of 5-lipoxygenase, shortly before percutaneous coronary intervention, reveals specific actions of leukotrienes on the heart rhythm. Inhibitors of 5-lipoxygenase might be of interest as a novel class of cardiac drugs affecting the conductive system.

18

Effects of ethanol and arachidonic acid pathway inhibitors on the effectiveness of gastric mucosa cytoprotection

63%

Lutnicki K., Szpringer E., Czerny K., Ledwozyw A.

Folia Morphologica

|

2001

|

tom 60

|

nr 1

Cytoprotection in the stomach, consisting in the mucus secretion, mucous circulation intensification and bicarbonate secretion to the gastric lumen, is highly dependent on the products of arachidonic acid pathway and peroxidative-antioxidative balance. The aim of the paper was to examine the effects of selected inhibitors of arachidonic acid pathway on the natural protective system of the gastric mucosa exposed to 50% ethanol. The results show that leukotrienes, thromboxane and oxygen reactive forms significantly impair the protective function of the gastric mucosa while prostaglandins and antioxidant enzymes act protectively.

19

The role of polymorphonuclear neutrophils in myocardial damage during ischemia and reperfusion

63%

Wysocki H.

Archivum Immunologiae et Therapiae Experimentalis

|

1992

|

tom 40

|

nr 1

20

NMDA receptors and nitric oxide regulate prostaglandin D2 synthesis in the rabbit hippocampus in vivo

63%

Lazarewicz J. W., Salinska E., Stafiej A., Ziembowicz A., Zieminska E.

Acta Neurobiologiae Experimentalis

|

2000

|

tom 60

|

nr 4

The aim of this in vivo microdialysis study was to characterise the regulation of prostaglandin D2 (PgD2) synthesis by NMDA receptors in the rabbit hippocampus in relation to changes in extracellular Ca concentration ([Ca ]e) and nitric oxide (NO) levels. Samples of dialysate were analysed for changes in PgD2 concentration, in [Ca ]e and in the level of NO. The results demonstrated that a 20-min pulse application of 0.1 - 2.5 mM NMDA via a microdialysis probe induced a prolonged stimulation of PgD2 release that was sensitive to competitive NMDA receptor antagonists. An inhibitor of voltage-sensitive Na+ channels, tetrodotoxin, did not influence this effect but significantly suppressed basal PgD2 production, whereas a NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), prevented NMDA-evoked NO release and inhibited NMDA-induced PgD2 release in an L-arginine-sensitive manner. NO donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside, stimulated PgD2 release. NMDA-evoked decrease in [Ca2+]e was insensitive to TTX and L-NAME. These results demonstrate an in vivo NMDA receptor-mediated modulation of PgD2 synthesis in the brain, in which NO participates.

Ograniczanie wyników

Tubular and vascular actions of cytochrome P450-arachidonate metabolites

Involvement of arachidonic acid and its products in the mechanism of progesterone influence on its own production in vitro in bovine corpus luteum

Nuclear import of arachidonate 5-lipoxygenase

The effect of the type and amount of fat in diet on the composition of fatty acids in tissue lipids in experimental hypercholesterolaemia

Cytochrome P-450 metabolites in renal circulation and excretion - interaction with nitric oxide [NO] system

Regulation of the NADPH oxidase activity and anti-microbial function of neutrophils by arachidonic acid

The effect of packed red blood cell storage on arachidonic acid and advanced glycation end-product formation

Production of prostacyclin and prostaglandin E2 in resting and IL-1beta-stimulated A549, HUVEC and hybrid EA.HY 926 cells

Modulation of NMDA receptor-mediated release of [3H]arachidonate in hippocampal slices of immature rats

Functional aspects of eicosanoid metabolism