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1

Characterization of proteins associating with 5' terminus of PGHS-1 mRNA

100%

Bunimov N., Laneuville O.

Cellular and Molecular Biology Letters

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2010

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tom 15

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nr 2

Induction of Prostaglandin Endoperoxide H Synthase-1 (PGHS-1) gene has been previously documented in a few studies during events such as development and cellular differentiation. However, molecular mechanisms governing the regulation of PGHS-1 gene expression and contributing to changes in protein levels are poorly understood. Using the MEG-01 cell model of PGHS-1 gene induction, our laboratory has previously demonstrated that the 5’UTR and the first two exons of PGHS-1 mRNA had a significant impact on decreasing the translational efficiency of a reporter gene and suggested that the presence of a secondary structure is required for conservation of this activity. This 5’end of PGHS-1 mRNA sequence has also been shown to associate with nucleolin protein. In the current study, we set to investigate the protein composition of the mRNP (messenger ribonucleoprotein) associating with the 5’end of PGHS-1 mRNA and to identify its protein members. RNA/protein binding assays coupled with LC-MS analysis identified serpin B1 and NF45 (nuclear factor 45) proteins as potential members of PGHS-1 mRNP complex. Immunoprecipitation experiments using MEG-01 protein extracts validated mass spectrometry data and confirmed binding of nucleolin, serpin B1, NF45 and NF90. The RNA fraction was extracted from immunoprecipitated mRNP complexes and association of RNA binding proteins, serpin B1, NF45 and NF90, to PGHS-1 mRNA target sequence was confirmed by RT-PCR. Together these data suggest that serpin B1, NF45 and NF90 associate with PGHS-1 mRNA and can potentially participate in the formation a single or a number of PGHS-1 ribonucleoprotein complexes, through nucleolin that possibly serves as a docking base for other protein complex members.

2

Resident peritoneal macrophages and mast cells are important cellular sites of COX-1 and COX-2 activity during acute peritoneal inflammation

100%

Kolaczkowska E., Goldys A., Kozakiewicz E., Lelito M., Plytycz B., Van Rooijen N., Arnold B.

Archivum Immunologiae et Therapiae Experimentalis

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2009

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tom 57

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nr 6

459-466

3

Antiangiogenic potential of grape stem extract through inhibition of vascular endothelial growth factor expression

100%

Stagos D., Apostolou A., Poulios E., Kermeliotou E., Mpatzilioti A., Kreatsouli K., Koulocheri S. D., Haroutounian S. A., Kouretas D.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 6

4

Effect of constitutive- and inducible-cyclooxygenase in the carbachol-induced pituitary-adrenocortical response during social stress

100%

Bugajski J., Gadek-Michalska A., Bugajski A. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 3

Acetylcholine potently stimulates the hypothalamic-pituitary-adrenal (HPA) axis. Cholinergic receptor agonist carbachol, given intraperitoneally (i.p.) or into the lateral cerebral ventricle (i.c.v.) to non-anesthetized rats acts via multiple pathways to stimulate the HPA axis. The present study sought to determine 1) the functional selectivity of carbachol for cholinergic muscarinic and/or nicotinic receptors involved in the stimulation of HPA axis; 2) the involvement of prostaglandins (PGs) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the carbachol-induced ACTH and corticosterone secretion in non-stressed rats and animals exposed to social crowding stress for 7 days (24 per a cage for 6). Carbachol was given i.c.v. or i.p. and cholinergic receptor antagonists or cyclooxygenase isoenzyme antagonists were given by the same routes 15 min earlier. One hour after the last injection trunk blood was taken for ACTH and corticosterone determinations. Atropine (0.1 µg i.c.v.), a cholinergic receptor antagonist, totally abolished the carbachol (2 µg i.c.v.)-induced ACTH and corticosterone secretion and mecamylamine (20 µg i.c.v.), a selective nicotinic receptor antagonist, did not affect this secretion. This finding indicates that carbachol functions as a selective central cholinergic muscarinic receptor agonist for the HPA axis stimulation. Crowding stress significantly diminished the carbachol (0.2 mg/kg i.p.)-induced plasma ACTH and corticosterone levels measured 1 hr after administration. Pretreatment with indomethacin (2 mg/kg i.p.), a non-selective cyclooxygenase inhibitor, significantly diminished the ACTH and corticosterone responses to carbachol (0.2 mg/kg i.p.) in control rats and moderately decreased these responses in stressed rats. Piroxicam (0.2 and 2.0 mg/kg i.p.), a COX-1 inhibitor, considerably impaired the carbachol-induced ACTH and corticosterone responses in control rats and markedly diminished these responses in stressed rats. A selective COX-2 blocker, compound NS-398 (0.2 and 2.0 mg/kg i.p.), substantially decreased the carbachol-induced hormones secretion in control rats but did not markedly alter this secretion in stressed rats. These results indicate that in the carbachol-induced HPA axis activation PGs generated by COX-1 are considerably and to a much greater extent involved than PGs generated by COX-2. Social stress markedly diminishes the mediation of PGs generated by COX-1 but PGs synthesized by COX-2 do not substantially participate in the carbachol-induced HPA response.

5

Effect of social stress on COX-1 and COX-2-induced alterations in the adrenergic agonists-evoked hypothalamic-pituitary-adrenal responses

100%

Bugajski J., Gadek-Michalska A., Glod R., Bugajski A. J.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,2

The purpose of the present study was to investigate the contribution of prostaglandins (PGs) synthesized by constitutive (COX-1) and inducible (COX-2) cyclooxygenase to stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic receptor agonists in rats under social crowing stress 3 days, (21 per a cage for 6) animals. The effects of phenylephrine, clonidine and isoprenaline, an alpha1-, alpha2- and ß-adrenergic agonist, respectively, in the presence and absence of COX-1 inhibitor, piroxicam, and COX-2 inhibitor, compound NS-398, on ACTH and corticosterone secretion in stressed rats were compared with these effects in non-stressed animals. All drugs were given intracerebroventricularly (i.c.v.), COX inhibitors 15 min before adrenergic agonists. Piroxicam (0.02 µg) and NS-398 (0.1 µg) significantly reduced the phenylephrine (30 µg) -induced ACTH and corticosterone secretion in both stressed and non-stressed rats. Piroxicam (0.02 µg) and NS-398 (0.01 µg) moderately decreased the clonidine (10 µg) -evoked hormone responses in control rats but did not alter these responses in stressed rats. Piroxicam (0.2 µg) and NS-398 (0.1µg) moderately diminished the isoprenaline (20 µg)-evoked ACTH and corticosterone response in control rats, while in stressed rats these inhibitors did not significantly alter the isoprenaline-induced rise in ACTH and corticosterone secretion. These results indicate that in hypothalamic structures involved in the regulation of adrenergic agonists-induced HPA stimulation COX-2 is expressed under physiological synaptic activity. Social crowding stress does not alter the significant involvement of prostaglandins in the HPA response induced by stimulation of central alpha1-adrenergic receptors. Prostaglandins are of lesser importance in activation of the HPA axis by alpha2-and ß-adrenergic receptors under basal and social stress conditions.

6

Prostaglandins and interleukin-1beta in the hypothalamic-pituitary-adrenal response to systemic phenylephrine under basal and stress conditions

84%

Gadek-Michalska A., Bugajski A. J., Bugajski J.

Journal of Physiology and Pharmacology

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2008

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tom 59

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nr 3

563-575

We investigated the role of interleukin-1ß (IL-1ß) and prostaglandins (PG) in the 1-adrenergic agonist, phenylephrine-induced hypothalamic-pituitary-adrenal axis (HPA) responses under basal and social stress conditions. Male Wistar rats, either control or exposed to crowding stress for 7 days prior to treatment, were used in these experiments. All compounds were injected i.p. Cyclooxygenase COX-1 and COX-2 inhibitors, piroxicam and compound NS-398, IL-1ß and IL-1ß receptor antagonist (IL-1ßRA) were injected 15 min before phenylephrine. Plasma ACTH and serum corticosterone levels were measured 1 h after phenylephrine or IL-1ß injection. Phenylephrine, in respective higher dose administered systemically (0.4 mg/kg i.p.) was almost equally effective as given i.c.v. (30 µg) in stimulating ACTH and corticosterone secretion. Likewise, the extent of the involvement of PG generated by COX-1 and COX-2 in the phenylephrine-induced ACTH and corticosterone secretion was similar after systemic or i.c.v. treatment under both resting and stress conditions. Piroxicam, stronger than compound NS-398, reduced the i.p. phenylephrine-induced ACTH and corticosterone secretion. IL-1ß receptor antagonist (50 µg/kg i.p.) did not significantly affect the inhibitory action of piroxicam on the i.p. phenylephrine-induced ACTH and corticosterone secretion in control rats, but significantly enhanced the inhibition evoked by piroxicam in stressed rats. IL-1ß (2.5 µg/kg i.p.) significantly increased ACTH and corticosterone secretion under basal conditions. Crowding stress for 7 days markedly impaired the IL-1ß-induced ACTH and corticosterone secretion. The mechanism of the stimulatory action of i.p. IL-1ß, which does not cross the blood-brain barrier, may comprise both central and peripheral components of the HPA axis. These results suggest that under basal conditions IL-1ß is not markedly involved in the 1-adrenergic agonist-induced stimulation of the HPA axis activity. During social crowding stress IL-1ß and prostaglandins are significantly involved in this stimulation.

7

Prostaglandins and ulcer healing

84%

Konturek S. J., Konturek P. C., Brzozowski T.

Journal of Physiology and Pharmacology. Supplement

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2005

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tom 56

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nr 5

5-31

Exogenous prostaglandins (PG) applied in small gastroprotective doses fail to affect healing of gastro-duodenal ulcers but accelerate the healing when used in larger gastric inhibitory doses that appear to enhance COX-2 expression and PGE2 generation in the ulcer area. COX-1 and COX-inhibitors delay ulcer healing, particularly when both COX isoforms are suppressed such e.g. by indomethacin. Dexamethasone, that decreases the expression of COX-2 and mucosal generation of PGE2, delays ulcer healing that can be reversed by the addition of small dose of exogenous PGE2. Proton pump inhibitors (PPI) such as omeprazole and PGE analogs, accelerate ulcer healing mainly due to potent inhibition of gastric acid secretion, but they also augment the COX-2 expression and enzyme activity in the ulcerated mucosa. Endogenous PG generated at ulcer margin appear to be involved in ulcer healing promoted by growth factors and gut hormones such as gastrin or CCK and melatonin acting, at least in part, through increase of induction of COX-2 and local release of PGE2 in the ulcer area . The ulcer healing activity of growth factors (e.g. EGF, TGFalpha, HGF) and certain gut hormones (gastrin, CCK) as well as melatonin, can be attenuated by treatment with COX-1 or COX-2 inhibitors which suppress the release of PGE2 but enhance the expression of COX-2. It is concluded that endogenous PG originating mainly from upregulated COX-2 at the ulcer margin play crucial role in ulcer healing by exogenous PG, PPI, growth factors, gut hormones and melatonin, while COX-1 and COX-2 inhibitors delay ulcer healing by suppressing PG generation, and increasing COX-2 expression in the ulcer area.

8

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.

9

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Hymenolepis diminuta - caused inflammation via the increased expression and activity of COX-1 and COX-2 in the rat jejunum and colon

84%

Kosik-Bogacka D., Baranowska-Bosiacka I., Kolasa-Wolosiuk A., Lanocha-Arendarczyk N., Gutowska I., Korbecki J., Namieta H., Rotter I.

Annals of Parasitology

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2016

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tom 62

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nr Suppl.

10

Role of COX inhibition in pathogenesis of NSAID-induced small intestinal damage

84%

Takeuchi K., Tanaka A., Ohno R., Yokota A.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

|

nr 4

165-182

Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin decrease mucosal PGE2 production by inhibiting cyclooxygenase (COX) activity and produce damage in the small intestine. The development of intestinal lesions as induced by indomethacin was accompanied by increases in intestinal motility, enterobacterial invasion, and myeloperoxidase (MPO) as well as inducible nitric oxide synthase (iNOS) activity, together with the up-regulation of COX-2 and iNOS mRNA expression. Neither the selective COX-1 inhibitor, SC-560, nor the selective COX-2 inhibitor, rofecoxib, alone caused intestinal damage, but their combined administration produced lesions. SC-560, but not rofecoxib, caused intestinal hypermotility, bacterial invasion and the expression of COX-2 as well as iNOS mRNAs, yet the iNOS and MPO activity was increased only when rofecoxib was administered together with SC-560. Although SC-560 inhibited the PG production, the level of PGE2 was recovered, in a rofecoxib-dependent manner. The intestinal hypermotility response to indomethacin was prevented by both 16,16-dimethyl PGE2 and atropine but not ampicillin, yet all these agents inhibited not only the bacterial invasion but also the expression of COX-2 as well as the iNOS activity in the intestinal mucosa following indomethacin treatment, resulting in preventing the intestinal lesions. These results suggest that inhibition of COX-1, despite causing intestinal hypermotility, bacterial invasion and iNOS expression, up-regulates the expression of COX-2, and the PGE2 derived from COX-2 counteracts deleterious events caused by COX-1 inhibition and maintains the mucosal integrity. These sequences of events explain why intestinal damage occurs when both COX-1 and COX-2 are inhibited.

11

Prostaglandins as mediators of COX-2 derived carcinogenesis in gastrointestinal tract

84%

Konturek P. C., Kania J., Burnat G., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2005

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tom 56

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nr 5

57-73

This review was designed to show the role of expression of cyclooxygenase (COX)-1 and COX-2 in the cancerogenesis of esophagus, stomach and colon. Unlike COX-1, which is expressed in the normal esophageo-gastro-colonic mucosa, COX-2 was found to be expressed mainly in the pre-cancer changes in the mucosa including Barrett's esophagus, Helicobacter pylori (H. pylori)-induced gastritis and inflammatory changes in colonic mucosa. In Barrett's esophagus, prostaglandins (PGs) derived from upregulated COX-2 contribute to the progression of low-grade to high-grade dysplasia and finally to cancer. In chronic gastritis induced by chronic H. pylori infection, overexpression of COX-2 is probably induced by inflammatory cytokines, growth factors, especially gastrin and reactive oxygen species leading to mutagenesis and subsequent metaplasia, dysplasia and cancer formation. The imbalance between cell proliferation and apoptosis caused mainly by products of COX-2 leads to cancerogenesis. Similarly, in colorectal cancer the overexpression of COX-2, possibly induced by the action of growth promoting factors including progastrin and gastrin and overexpression of survivin contribute to the colorectal cancerogenesis that could be, at least in part, amended by the treatment with specific COX-2 inhibitors. We conclude that: 1) COX-2-derived PGs play a key role in the tumorogenesis in the gastrointestinal tract; 2) The tumor-promoting effect of PGs may be attributed to their ability to stimulate cell proliferation and migration, to inhibit the apoptosis and to increase angiogenesis and invasiveness; 3) In accordance to the proposed major role of COX-2 in cancerogenesis, selective COX-2 inhibitors have been shown in numerous studies to exhibit strong chemopreventive effect on the development of gastrointestinal cancers.

12

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

|

nr 4

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.

13

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

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.

14

Involvement of cyclooxygenase (COX)-2 products in acceleration of ulcer healing by gastrin and hepatocyte growth factor

84%

Brzozowski T., Konturek P. C., Konturek S. J., Pajdo R., Schuppan D., Drozdowicz D., Ptak A., Pawlik M., Nakamura T., Hahn E. G.

Journal of Physiology and Pharmacology

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2000

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tom 51

|

nr 4,1

15

Involvement of prostaglandins in the nicotine-induced pituitary-adrenocortical response during social stress

84%

Bugajski J., Gadek-Michalska A., Bugajski A. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

|

nr 4,2

The present study examined the functional selectivity of nicotine for nicotinic acetylcholine receptors in the stimulation of the hypothalamic-pituitary-adrenal (HPA) axis, the effect of social crowding stress on HPA response to nicotine and the involvement of prostaglandins synthesized by constitutive cyclooxygenase (COX-1) and inducible cyclooxygenase (COX-2) in the nicotine-induced HPA response in rats crowded (24 per a box instead 7) for 7 days. Nicotine (2.5-5.0 mg/kg i.p.) significantly increased plasma ACTH and corticosterone levels measured 1 h after administration. Mecamylamine (50 mg i.c.v.), a selective nicotinic receptor antagonist, atropine (0.1 mg/kg i.p.) a non-selective cholinergic receptor antagonist, or COX inhibitors were injected 15 min prior to nicotine and the rats were decapitated 1 h after the last injection. Mecamylamine abolished the nicotine-induced ACTH response and significantly diminished corticosterone response. Atropine did not alter ACTH response and modestly diminished corticosterone response to nicotine. Crowding stress significantly impaired the nicotine-evoked ACTH and corticosterone secretion. Pretreatment with piroxicam (0.2-2.0 mg/kg), a COX-1 inhibitor, considerably diminished the nicotine-induced ACTH and corticosterone secretion in control and crowded rats. Compound NS-398 (0.2-5.0 mg/kg), a selective COX-2 blocker, did not markedly alter the nicotine-induced hormones secretion in either control or stressed rats. Indomethacin (2 mg/kg), a non-selective COX inhibitor diminished significantly, but to a lesser extent than piroxicam, the nicotine-stimulated ACTH and corticosterone response. These results indicate that systemic nicotine stimulates the HPA axis selectively via nicotinic acetylcholine receptors. Chronic social stress significantly impairs the nicotine stimulated ACTH and corticosterone secretion. Prostaglandins, generated by COX-1- but not by COX-2- isoenzyme, are of crucial significance in the nicotine-induced ACTH and corticosterone secretion in both control and stressed rats.

16

Influence of cyclooxygenase inhibitors on the central histaminergic stimulation of hypothalamic-pituitary-adrenal axis

84%

Bugajski A. J., Thor P., Glod R., Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

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2003

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tom 54

|

nr 4

Brain histamine participates in central regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Endogenous prostaglandins modulate signal transduction of different neurotransmitters involved in activation of HPA axis. In the present experiment we investigated whether endogenous prostaglandins are involved in the stimulation of ACTH and corticosterone secretion by histaminergic systems in the rat brain. Histamine (50 µg), histamine-trifluoromethyl-toluidine derivative (HTMT, 75 µg) a selective and potent H1-receptor agonist, and amthamine (50 µg) a H2-receptor agonist given intracerebroventricularly (i.c.v.) to non-anesthetized rats considerably increased ACTH and corticosterone secretion 1h after administration. A non-selective cyclooxygenase inhibitor indomethacin (2 mg/kg i.p. or 10 µg i.c.v.), piroxicam (0.02 and 0.2 µg i.c.v.) a more potent antagonist of constitutive cyclooxygenase (COX-1) and compound NS-398 (0.1 and 1.0 µg i.c.v.), a selective inhibitor of inducible cyclooxygenase (COX-2) were given 15 min before histamine and histamine receptor agonists. One hour after the last injection trunk blood from decapitated rats was collected for hormones determination. The histamine-induced ACTH and corticosterone secretion was significantly diminished by piroxicam and was not markedly altered by indomethacin and compound NS-398. The HTMT-elicited increase in ACTH and corticosterone secretion was significantly prevented by indomethacin and was not affected by piroxicam or compound NS-398. The amthamine-evoked increase in ACTH and corticosterone secretion was not markedly influenced by any cyclooxygenase blocker applied in the present experiment. These results indicate that the histamine H1-receptor transmitted central stimulation of the HPA axis is considerably mediated by prostaglandins generated by consititutive cyclooxygenase, whereas stimulation transmitted via H2-receptor does not significantly depend on endogenous prostaglandins mediation.

17

Effect of cyclooxygenase inhibitors on the CRH-induced pituitary-adrenocortical activity during crowding stress

84%

Bugajski J., Gadek-Michalska A., Bugajski A. J.

Journal of Physiology and Pharmacology

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2003

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tom 54

|

nr 1

The aim of the present study was to determine the effect of social stress and significance of prostaglandins (PG) generated by constitutive and inducible cyclooxygenase (COX-1 and COX-2) in the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by corticotropin releasing hormone (CRH) under basal and social crowding stress conditions. The stressed rats were crowded in groups of 24 to a cage for 3 or 7 days, whereas the control animals were haused in groups of 7 to a cage of the same size. The activity of HPA axis was determined by measuring plasma ACTH and serum corticosterone levels 1 h after i.p. CRH administration. Inhibitors of COX-1, piroxicam (0.2, 2.0, and 5.0 mg/kg), and COX-2, compound NS-398 (0.2 and 2.0 mg/kg), were administered i.p. 15 min prior to CRH (0.1 µg/kg i.p.) to control or crowded rats. The obtained results indicate that social stress for 3 and 7 days markedly intensifies the stimulatory action of CRH on ACTH secretion. Neither piroxicam nor NS-398 induce any significant effect on the CRH-elicited ACTH and corticosterone secretion in non-stressed or crowded rats. Therefore, PG generated by COX-1 or COX-2 do not participate to a significant extent in the stimulation of HPA axis by CRH under either basal conditions or during crowding stress. These results also indicate that the stimulatory action of CRH on ACTH secretion is not only completely resistant to desensitization but is sensitized during social crowding stress. The results contrast with a significant involvement of PG in the vasopressin-induced stimulation of HPA response during crowding stress.

18

Anti-inflammatory effects of nesfatin-1 on acetic acid-induced gastric ulcer in rats: involvement of cyclo-oxygenase pathway

67%

Kolgazi M., Ozdemir-Kumral Z. N., Cantali-Ozturk C., Demirci E. K., Yuksel M., Sirvanci S., Yegen B. C.

Journal of Physiology and Pharmacology

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2017

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tom 68

|

nr 5

19

Inhibitors of cyclooxygenases: mechanisms, selectivity and uses

67%

Botting R. M.

Journal of Physiology and Pharmacology. Supplement

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2006

|

tom 57

|

nr 5

113-124

The prostaglandins are lipid mediators, discovered in the 1930s by von Euler in Sweden and Goldblatt in the United Kingdom. They are made by the bifunctional enzyme, cyclooxygenase, which has both cyclooxygenase and peroxidase activities in the same molecule. Prostaglandins are involved in physiological functions such as protection of the stomach mucosa, aggregation of platelets and regulation of kidney function. They also have pathological functions such as their involvement in inflammation, fever and pain. Vane in 1971 elegantly showed that the pharmacological actions of aspirin and similar drugs were due to the inhibition of cyclooxygenase. Thus, aspirin-like drugs exert their anti-inflammatory, antipyretic and analgesic effects by inhibition of cyclooxygenase. In 1991, Simmons and his colleagues identified a second cyclooxygenase enzyme, designated cyclooxygenase-2, derived from a separate gene from cyclooxygenase-1. Cyclooxygenase-2 is upregulated by inflammatory mediators and forms prostaglandins which intensify the inflammatory response. Cyclooxygenase-1 is, therefore, a 'housekeeping' enzyme making prostaglandins, which are important for maintaining physiological functions and cyclooxygenase-2 makes prostaglandins which are important in inflammation. The discovery of cyclooxygenase-2 and the establishment of its structure led to the development of selective inhibitors of this enzyme, such as celecoxib and rofecoxib, with potent anti-inflammatory actions but with reduced gastrotoxic effects. A putative cyclooxygenase-3, has also been characterised and cloned. This enzyme is a product of the cyclooxygenase-1 gene, but retains intron 1 after transcription and translates into a cyclooxygenase enzyme with 34 additional amino acids. It is more sensitive to inhibition by paracetamol, aspirin and some other non-steroid anti-inflammatory drugs than cyclooxygenase-1 or cyclooxygenase-2. A cyclooxygenase enzyme induced in cultured cells by some non-steroid anti-inflammatory drugs is also more sensitive to inhibition by paracetamol than cyclooxygenase-2 induced by bacterial lipopolysaccharide

20

Analysis of 18S rRNA, ITS2 and cox1 sequences of Dictyocaulus spp. (Trichostrongyloidea: Dictyocaulidae) from the European bison, roe deer and red deer in Poland: molecular evidence for a new species

67%

Pyziel A. M., Laskowski Z., Demiaszkiewicz A. W., Hoglund J.

Annals of Parasitology

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2016

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tom 62

|

nr Suppl.

Ograniczanie wyników

Characterization of proteins associating with 5' terminus of PGHS-1 mRNA

Resident peritoneal macrophages and mast cells are important cellular sites of COX-1 and COX-2 activity during acute peritoneal inflammation

Antiangiogenic potential of grape stem extract through inhibition of vascular endothelial growth factor expression

Effect of constitutive- and inducible-cyclooxygenase in the carbachol-induced pituitary-adrenocortical response during social stress

Effect of social stress on COX-1 and COX-2-induced alterations in the adrenergic agonists-evoked hypothalamic-pituitary-adrenal responses

Prostaglandins and interleukin-1beta in the hypothalamic-pituitary-adrenal response to systemic phenylephrine under basal and stress conditions

Prostaglandins and ulcer healing

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

Hymenolepis diminuta - caused inflammation via the increased expression and activity of COX-1 and COX-2 in the rat jejunum and colon

Role of COX inhibition in pathogenesis of NSAID-induced small intestinal damage

Prostaglandins as mediators of COX-2 derived carcinogenesis in gastrointestinal tract

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

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

Involvement of cyclooxygenase (COX)-2 products in acceleration of ulcer healing by gastrin and hepatocyte growth factor

Involvement of prostaglandins in the nicotine-induced pituitary-adrenocortical response during social stress

Influence of cyclooxygenase inhibitors on the central histaminergic stimulation of hypothalamic-pituitary-adrenal axis

Effect of cyclooxygenase inhibitors on the CRH-induced pituitary-adrenocortical activity during crowding stress

Anti-inflammatory effects of nesfatin-1 on acetic acid-induced gastric ulcer in rats: involvement of cyclo-oxygenase pathway

Inhibitors of cyclooxygenases: mechanisms, selectivity and uses

Analysis of 18S rRNA, ITS2 and cox1 sequences of Dictyocaulus spp. (Trichostrongyloidea: Dictyocaulidae) from the European bison, roe deer and red deer in Poland: molecular evidence for a new species