Wyniki wyszukiwania - Biblioteka Nauki

1

Is the prostaglandin E2 responsible for pyrogen fever centrally or peripherally derived?

100%

Milton A. S.

Acta Physiologica Polonica

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1990

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tom 41

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nr 1-3

2

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

100%

Olszanecki R. , Gebska A. , Korbut R.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 4

EN

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.

3

The role of tyrosine kinase in prostaglandin E2 and vanadate-evoked contractions in rabbit duodenum in vitro

100%

Grasa L. , Arruebo M. P. , Plaza M. A. , Murillo M. D.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 2

EN

Prostaglandin E2 (PGE2) can interact with at least four cell surface receptors (EP1-EP4) in smooth muscle, which evokes a variety of intracellular responses depending on the G protein to which the cell surface receptors are coupled. The activation of G protein-coupled receptors and receptor tyrosine kinases can lead to the phosphorylation of tyrosine residues of various cellular proteins. The aim of this study was to examine the role of tyrosine phosphorylation in PGE2, vanadate and carbachol-evoked contractions. PGE2, vanadate, and carbachol induced contractile motor responses in the longitudinal smooth muscle of rabbit duodenum. PGE2-evoked contractions decreased in the presence of genistein or tyrphostin B44. PGE2-evoked contractions increased in the presence of vanadate. Vanadate-evoked contractions decreased in the presence of genistein. In contrast, tyrphostin 47 increased the vanadate-evoked contractions. Vanadate-evoked contractions were reduced in the presence of Ca2+-free solutions, verapamil, or indomethacin. U-73122 decreased PGE2-evoked contractions. Carbachol-evoked contractions decreased in the presence of genistein, tyrphostin B44 or tyrphostin 47. Our results suggest that PGE2, vanadate or carbachol-evoked contractions are mediated by protein tyrosine phosphorylation. Protein tyrosine phosphorylation might cause an increase in calcium influx through voltage-dependent channels and the release of prostaglandins in the longitudinal smooth muscle of the rabbit duodenum.

4

Prophylactic potential of montelukast against mild colitis induced by dextran sulphate sodium in rats

100%

Holma R. , Salmenpera P. , Virtanen I. , Vapaatalo H. , Korpela R.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 3

EN

Cysteinyl leukotrienes play a part in inflammatory processes such as inflammatory bowel diseases. The present study aimed to evaluate the effects of the cys-LT-1 receptor antagonist montelukast on a mild colitis model in rats. Colitis was induced by administrating 4% dextran sulphate sodium (DSS, MW 45 000) in drinking water for 9 days. Montelukast (10 mg/kg/day) or vehicle was given by gastric gavage once daily simultaneously with DSS administration. A healthy control group receiving water as drinking fluid and vehicle by gastric gavage was included. Body weight loss, consistency of faeces (loose/diarrhoea) and occult blood in the faeces/ gross bleeding were assessed on days 6 - 9. After sacrifice, the following were assessed: colonic histology, the expression of inducible nitric oxide synthase, macrophage/monocyte marker ED1, cyclooxygenase-1 and cyclooxygenase-2, as well as the production of leukotriene B4 and E4, prostaglandin E2, its metabolite bicyclic-prostaglandin E2 and thromboxane B2 in the colonic tissue incubation in vitro. Rats receiving DSS exhibited bloody diarrhoea from day 6 onwards. Montelukast significantly reduced the occult blood in the faeces/ gross bleeding, maintained normal body weight gain and tended to decrease the ratio of leukotriene B4/ prostaglandin E2 production in the colon in vitro. The results indicate that montelukast has some potential to ameliorate mild experimental colitis induced by DSS.

5

Prostaglandin D2 produced by hematopoietic prostaglandin D synthase contributes to LPS-induced fever

84%

Gao W. , Schmidtko A. , Wobst I. , Lu R. , Angioni C. , Geisslinger G.

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tom 60

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nr 2

145-150

EN

A large body of evidence has implicated prostaglandin E2 (PGE2) in fever production. However, the role of PGD2 in this context is only poorly understood. We therefore determined by LC-MS/MS analyses the content of PGD2 and PGE2 in cerebrospinal fluid (CSF), plasma and lungs of rats over 5 hours after fever induction by intraperitoneal injection of lipopolysaccharide (LPS, 50 µg/kg). Both PGD2 and PGE2 were detected in CSF, plasma and lungs of saline-treated control animals. The injection of LPS evoked fever and an increase of PGE2 in the CSF, while the CSF content of PGD2 was not significantly altered. However, both PGE2 and PGD2 levels were elevated in plasma and lungs after LPS injection. Interestingly, pretreatment with a novel selective inhibitor of hematopoietic prostaglandin D synthase (H-PGDS), EDJ300520 (10-40 mg/kg p.o.), selectively and dose-dependently prevented the LPS-induced increase of PGD2 in plasma and lungs but did not affect the PGE2 content. Most remarkably, EDJ300520 pretreatment led to an hypothermic response after LPS injection during the first 3 h and prevented fever induction. These data indicate that PGD2 produced peripherally by H-PGDS essentially contributes to LPS-induced fever.

6

Role of prostaglandins in heme-induced fever

84%

Walentynowicz K. , Szefer M. , Wojtal B. , Terlecki P. , Wrotek S. , Kozak W.

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nr 8

73-82

EN

Brain stroke is often accompanied by a high fever, which is insensitive to a blockade with classic antipyretic drugs known to inhibit the synthesis of prostaglandin E2 (PGE2), a proximal mediator of fever associated with infection. The molecular mechanism of fever associated with stroke is mostly unknown, and has not been thoroughly investigated. One characteristics of the stroke is an extravasation of the erythrocytes into the brain tissue followed by a release of hemoglobin and free heme. In the present study we have tested the hypothesis that free heme itself can induce fever after releasing into the brain. The study was conducted on Sprague Dawley rats instrumented with biotelemetry devices to monitor deep body temperature, and implanted with brain cannulae projected to the lateral ventricle. We demonstrate that heme-L-lysinate microinfused intraventricularly (icv) induces a dose-dependent fever lasting ca. 8 hours. Injection of heme-L-lysinate provoked a significant elevation of PGE2 in the rat cerebro-spinal fluid collected 3 hours post-injection. The fever induced by heme-L-lysinate was blocked by an icv injection of anti- PGE2 antibody. It was not affected, however, by intraperitoneal administration of indomethacin, a cyclooxygenase inhibitor. We conclude that heme-induced fever may underlie the stroke fever.

7

Arecoline inhibits interleukin-2 secretion in Jurkat cells by decreasing the expression of alpha7-nicotinic acetylcholine receptors and prostaglandin E2

84%

Hwang G. S. , Hu S. , Lin Y. H. , Chen S. T. , Tang T. K. , Wang P. S. , Wang S. W.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 5

8

Puerperal influence of bovine uterine health status on the mRNA expression of pro-inflammatory factors

84%

Peter S. , Michel G. , Hahn A. , Ibrahim M. , Lubke-Becker A. , Jung M. , Einspanier R. , Gabler C.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 3

9

Comparison between the effects of lisinopril and losartan on the cough reflex in anesthetized and awake rabbits

84%

Mutolo D. , Cinelli E. , Bongianni F. , Evangelista S. , Pantaleo T.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 2

10

Role of epidermal growth factor receptor transactivation in the activation of cytosolic phospholipase A2 in leptin protection of salivary gland acinar cells against ethanol cytotoxicity

84%

Slomiany B. L. , Slomiany A.

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tom 60

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nr 2

49-55

EN

A pleiotropic hormone, leptin, secreted into saliva by the acinar cells of salivary glands is an important mediator of the processes of oral mucosal defense. Here, we report on the role of epidermal growth factor receptor (EGFR) transactivation in the signaling events that mediate leptin protection of sublingual salivary gland acinar cells against ethanol cytotoxicity. We show that the protective effect of leptin against ethanol cytotoxicity was associated with the increased EGFR protein tyrosine kinase and cytosolic phospholipase A2 (cPLA2) activity, and characterized by a marked increase in matrix metalloproteinase MMP-9 and arachidonic acid (AA) release, and PGE2 generation. The loss in countering capacity of leptin against ethanol cytotoxicity was attained with JAK inhibitor AG490, Src inhibitor PP2, and EGFR inhibitor AG1478, as well as ERK inhibitor PD98059. Moreover, the agents evoked also the inhibition in leptin-induced up-regulation in cPLA2 activity, AA release, and PGE2 generation. The changes caused by leptin in EGFR phosphorylation, MMP-9, and cPLA2 activation were susceptible to suppression by metalloprotease inhibitor GM6001, but the production of MMP-9 was not affected by EGFR inhibitor AG1478 or PKC inhibitor Ro318220. These findings point to the involvement of MMP-9 in the event of leptin-induced EGFR transactivation that results in the signaling cascade leading to cPLA2 activation and up-regulation in PGE2 generation, thus providing new insights into the mechanism of oral mucosal protection against ethanol toxicity.

11

The role of local and systemic cytokines in patients infected with Clostridium difficile

84%

Czepiel J. , Biesiada G. , Brzozowski T. , Ptak-Belowska A. , Perucki W. , Birczynska M. , Jurczyszyn A. , Strzalka M. , Targosz A. , Garlicki A.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 5

12

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.

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tom 60

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nr 1

77-85

EN

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.

13

Effects of rosmarinic acid on cognitive and biochemical alterations in ovariectomized rats treated with D-galactose

84%

Gok D. K. , Ozturk N. , Er H. , Aslan M. , Demir N. , Derin N. , Agar A. , Yargicoglu P.

Folia Histochemica et Cytobiologica

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2015

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tom 53

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nr 4

14

Time-dependent supplementation of vitamin E influences leptin expression in the aortic layers of rats fed atherogenic diet

84%

Krawczynska A. , Olczak E. , Rembiszewska A. , Herman A. P. , Gromadzka-Ostrowska J.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 1

15

The cyclooxygenase-2/prostaglandin E2 pathway and its role in the pathogenesis of human and dog hematological malignancies

84%

Zmigrodzka M. , Rzepecka A. , Krzyzowska M. , Witkowska-Pilaszewicz O. , Cywinska A. , Winnicka A.

Journal of Physiology and Pharmacology

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2018

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tom 69

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nr 5

16

Testing and typing of eicosanoid-patterns

84%

Schafer D.

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tom 57

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nr 12

47-64

EN

Eicosanoids are pleiotrope mediators with essential function in most biological processes. The network of inter- and intracellular signalling requires coordinated cellular information processing. The cross-talk is characterised by complex non-linear responses to combinations of different stimuli and cells, but little is known about the density of these interactions. Here I have analysed eicosanoid interactions carried out by functional eicosanoid testing and typing (FET) in leucocytes from healthy subjects and patients suffering from inflammatory diseases. The known eicosanoid pattern scoring was extended to metabolically linked prostaglandin E2 and peptido-leukotrienes pathways, both alone and in all pair wise combinations, for basal, maximal synthesis capacity, acetylsalicylic acid, and neuropeptide modification. Eicosanoids fluctuated over twenty minutes context-dependent dynamically, demanding further data integration. The integration suggested that many stimuli converge for quantitative discrimination applying a total eicosanoid pattern score (TEP). Varying cellular activities affect FET and thereby TEP. The non-additive metabolic interactions were consistent with known mechanisms of metabolic pathway cross-talk. FET-based modelling of eicosanoid circuits most suitably reflects the fundamental impact of eicosanoids in maintaining cellular integrity of organ and body function. This might improve our present understanding of complex cellular eicosanoid interactions of inflammatory diseases and might be applied for diagnostic considerations.

17

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

84%

Jawien J. , Olszanecki R. , Lorkowska B. , Korbut R.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 4

EN

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.

18

Characterization of 'unhealed gastric ulcers' produced with chronic exposure of acetic acid ulcers to indomethacin in rats

84%

Amagase K. , Yokota M. , Tsukimi Y. , Okabe S.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 3

EN

We previously discovered that a 4-wk course of indomethacin delivered to rats with acetic acid ulcers resulted in production of "unhealed gastric ulcers" that persisted for up to 12 wks after treatment cessation. The present study examined the mechanism underlying such "unhealed gastric ulcers" with biochemical and histological procedures. "Unhealed gastric ulcers" were induced with a 4-wk indomethacin treatment (1 mg/kg, twice daily) in rats with acetic acid ulcers. Two and 4 wks after treatment cessation, ulcer size was significantly larger in rats receiving indomethacin compared with control animals. Ulcerated tissue prostaglandin E2 levels were significantly lower during indomethacin treatment, but the levels tended to increase after treatment cessation compared with levels measure in the group receiving vehicle. Myeloperoxidase activity levels were significantly higher during indomethacin treatment; such levels persisted after treatment cessation. Histologically, greater degrees of fibrosis and neutrophil accumulation, as well as a lesser degree of angiogenesis were observed in the "unhealed gastric ulcers" compared to ulcers that healed in a normal fashion. It was concluded that severe fibrosis, persistent neutrophil infiltration, and poor angiogenesis in the ulcer base might represent factors involved in the mechanism underlying production of "unhealed gastric ulcers".

19

Deficiency of cyclooxygenases transcripts in cultured primary bronchial epithelial cells of aspirin-sensitive asthmatics

84%

Pierzchalska M. , Soja J. , Wos M. , Szabo Z. , Nizankowska-Mogilnicka E. , Sanak M. , Szczeklik A.

Journal of Physiology and Pharmacology

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2007

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tom 58

|

nr 2

EN

Background Airway function is actively regulated by epithelium through generating PGE2, the production of which depends on cyclooxygeneses (COX-1 and COX-2). Analysis of bronchial biopsies and bronchial epithelial cells in culture conducted so far gave conflicting results of expression pattern of these enzymes in healthy subjects and asthmatics patients, with and without aspirin hypersensitivity. Objective Our aim was to investigate the expression of COX-1 and COX-2 mRNA in primary human bronchial epithelial cells (HBEC) isolated from asthmatics and non-asthmatics. Methods We isolated HBEC from bronchial brushing preparations taken during bronchoscopy of 10 non-asthmatics (NA), 8 aspirin-tolerant asthmatics (ATA) and 9 aspirin-intolerant asthmatics (AIA). HBEC were cultured in serum free medium until 80% confluent. Total cellular RNA was isolated and reversed transcribed using oligo(dT)15 primers. Real time PCR was performed with primers to COX-1, COX-2, GAPDH and ß-actin in the presence of SYBR green dye. The cycle threshold (CT) for COX-1 or COX-2 was normalized using ß-actin and GAPDH as the internal standards. Results Not only COX-1 but also COX-2 mRNA were expressed by HBEC without any proinflammatory stimulation. We detected the smallest amount of COX-1 mRNA in the AIA group. The same trend was observed for COX-2 mRNA, though it didn’t reach the statistical significance. We also analysed the relationship between CTCOX-1 to CTCOX-2 by calculating the difference DCTCOX-1-COX-2. This analysis revealed that AIA group can be characterized by relatively smallest COX-1 mRNA expression in comparison to COX-2. There is a strong positive correlation between CTCOX1 and CTCOX2 in NA group (r=0.85; p< 0.001). In both groups of asthmatics this correlation is absent (ATA – r=0.5, p>0.1; AIA – r=0.43, p>0.1). Conclusions Cyclooxygeneases transcripts expression is altered in HBEC derived from the asthmatic patients, and this phenomenon is pronounced in case of aspirin hypersensitivity.

20

Involvement of cyclooxygenase-1, prostaglandin E2 and EP1 receptors in acid-induced HCO3- secretion in stomach

84%

Takeuchi K. , Aihara E. , Sasaki Y. , Nomura Y. , Ise F.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 4

EN

We investigated the cyclooxygenase (COX) isoforms as well as prostaglandin E receptor EP subtypes responsible for acid-induced gastric HCO3- secretion in rats and EP receptor-knockout (-/-) mice. Under urethane anesthesia, a chambered stomach (in the presence of omeprazole) was perfused with saline, and HCO3-secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Mucosal acidification was achieved by exposing the stomach for 10 min to 50 or 100 mM HCl. Acidification of the mucosa increased the secretion of HCO3- in the stomach of both rats and WT mice, in an indomethacin-inhibitable manner. The acid-induced gastric HCO3- secretion was inhibited by prior administration of indomethacin and SC-560 but not rofecoxib in rats and mice. Acidification increased the PGE2 content of the rat stomach, and this response was significantly attenuated by indomethacin and SC-560 but not rofecoxib. This response was also attenuated by ONO-8711 (EP1 antagonist) but not AE3-208 (EP4 antagonist) in rats and disappeared in EP1 (-/-) but not EP3 (-/-) mice. PGE2 increased gastric HCO3- secretion in both rats and WT mice, and this action was inhibited by ONO-8711 and disappeared in EP1 (-/-) but not EP3 (-/-) mice. These results support a mediator role for endogenous PGs in the gastric response induced by mucosal acidification and clearly indicate that the enzyme responsible for production of PGs in this process is COX-1. They further show that the presence of EP1 receptors is essential for the increase in the secretion of HCO3- in response to mucosal acidification in the stomach.