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

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1993

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tom 44

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nr 2

2

Physiological mediators in nonsteroidal anti-inflammatory drugs (NSAIDs)-induced impairment of gastric mucosal defense and adaptation. Focus on nitric oxide and lipoxins

88%

Brzozowski T., Konturek P. C., Pajdo R., Ptak-Belowska A., Kwiecien S., Pawlik M., Drozdowicz D., Sliwowski Z., Brzozowski B., Konturek S. J., Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

|

nr 2

Prostaglandins mediate various physiological aspects of mucosal defense and the suppression of prostaglandin synthesis in the stomach is a critical event in terms of the development of mucosal injury after NSAID administration. However, it has become clear that other mediators besides prostaglandins can similarly act to protect the stomach from injury. For instance, nitric oxide (NO) released from vascular epithelium, epithelial cells of gastrointestinal tract and sensory nerves can influence many of the same components of mucosal defense as do prostaglandins. Thus, administration of NO in a form of NO-donors exert protective influence on the stomach from the injury that usually occurs when mucosal prostaglandin levels are suppressed. The new class of NO releasing NSAIDs, including NO-aspirin, represent a very promising approach to reducing the toxicity of anti-inflammatory drugs. Lipoxins are another group of lipid mediators that can protect the stomach. Aspirin-triggered lipoxin synthesis, via COX-2, acts to reduce the severity of damage induced by this drug. Lipoxin analogues may prove to be useful for preventing mucosal injury and for modulating mucosal inflammation. Aspirin-triggered lipoxin also seems to play in important role in gastric adaptation during chronic aspirin administration. Suppression of COX-2 activity by selective COX-2 inhibitors abolishes the production of this endogenous gastroprotective substance and diminishes the gastric tolerability of NSAIDS and gastric adaptation to these drugs. This review was designed to give an updated overview on the physiological factors and experimental and clinical attempts that were used or may be used in the future as the therapeutic approach to counteract adverse effects in the stomach associated with NSAID ingestion.

3

Cyclooxygenase pathways

75%

Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.

Acta Biochimica Polonica

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2014

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tom 61

|

nr 4

4

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

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2008

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tom 59

|

nr 9

137-149

5

Effects of indomethacin and rofecoxib on gastric mucosal damage in normal and Helicobacter pylori - infected Mongolian gerbils

75%

Kanatani K., Ebata M., Murakami M., Okabe S.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,2

This study examined the effects of indomethacin and rofecoxib on normal and Helicobacter pylori (H. pylori)-infected gastric mucosa of Mongolian (M.) gerbils. M. gerbils (6-wk-old) were orally administered H. pylori (ATCC43504, 2×108 CFU/ml) after fasting for 24 hours. Beginning 3 mo after inoculation, indomethacin (2 mg/kg, s.c) or rofecoxib (10 mg/kg, p.o.) was administered once daily for 2 wk to the gerbils. At autopsy, gastric mucosal ulcer area, myeroperoxidase (MPO) activity, prostaglandin (PG) E2 synthesis, and H. pylori viability were determined. Histamine-stimulated gastric acid secretion was measured with the acute gastric fistula method. Histological study was performed with H&E staining. H. pylori infection caused severe mucosal damage and production of lymphoid follicles in the gastric submucosa. In H. pylori-infected gerbils, indomethacin aggravated the gastric mucosal damage induced by H. pylori infection. Furthermore, indomethacin by itself induced gastric ulcers at an incidence of 6/10. In contrast, rofecoxib did not aggravate the H. pylori-induced mucosal damage. Indomethacin and rofeocoxib significantly reduced H. pylori viability. MPO activity was significantly increased in H. pylori-infected gerbils compared with H. pylori-uninfected gerbils. Indomethacin and rofecoxib reduced MPO activity in H. pylori-infected gerbils. PGE2 synthesis was markedly increased in H. pylori-infected gerbils (approximately 3-times) compared with the normal gerbils. Indomethacin significantly inhibited PGE2 synthesis in the gastric mucosa, both in normal and H. pylori-infected gerbils. Rofecoxib did not reduce PGE2 synthesis in normal gerbils, however, PGE2 synthesis was reduced to normal levels in H. pylori-infected gerbils. In H. pylori-infected gerbils, histamine-stimulated gastric acid secretion was reduced compared with normal gerbils. Indomethacin significantly increased histamine-stimulated gastric acid secretion and rofecoxib tended to increase secretion in H. pylori-infected gerbils. It was concluded that indomethacin enhances development of gastric mucosal damage in normal gerbils and aggravates H. pylori-induced gastric damage, resulting in gastric ulcers. Rofecoxib did not induce gastric damage in normal gerbils and did not aggravate damage in H. pylori-infected gerbils, suggesting that rofecoxib is less damaging to the stomach than indomethacin.

6

Interleukin 1beta induces functional prostaglandin E synthase in cultured human umbilical vein endothelial cells

75%

Uracz W., Uracz D., Olszanecki R., Gryglewski R. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

|

nr 4,1

Prostaglandin endoperoxide H2 (PGH2) is generated from arachidonic acid by either constitutive (COX-1) or inducible (COX-2) cyclooxygenases. In arterial wall PGH2 is converted by PGI2 synthase (PGI-S) to prostacyclin (PGI2), and in platelets by thromboxane synthase (TX-S) to thromboxane (TXA2). Other prostanoids as PGD2, PGF2alpha or PGE2 were believed to arise non-enzymatically from PGH2. Only recently, human prostaglandin E synthase (PGE-S) has been identified and cloned as a membrane bound, microsomal, glutathione-dependent inducible enzyme. Here we demonstrated that interleukin 1ß (IL-1ß) is an inducer of COX-2 and PGE-S in human umbilical vein endothelial cells (HUVEC). Functional expression of PGE-S was measured at the level of specific mRNA by semi-quantitative RT-PCR, PGE-S protein was detected by Western blot in HUVEC, while PGE2 was measured by immunoassay in the supernatant. Actinomycin D, a classical transcription inhibitor, was used to prove that indeed IL-1ß induced the functional PGE-S enzyme. PGE2 generation in HUVEC was inhibited by indomethacin, acetamoniphen and dexamethasone. In conclusion, we found that in cultured endothelial cells IL-1ß induced as evidenced by the appearance of its transcript and its functional enzyme. The induction of endothelial PGE-S and COX-2 appeared to be and their transcripts were induced as fast as one might expect from immediate early genes. It means that IL-1ß-triggered-PGE2 biosynthesis in endothelial cells is probably regulated by induction of both COX-2 and PGE-S. This is way we hypothesise the existence of at least two distinct pools of COX-2: the first selectively coupled to PGE-S and the second one that is coupled to PGI-S yielding the main endothelial product - PGI2.

7

Involvement of constitutive (COX-1) and inducible cyclooxygenase (COX-2) in the adrenergic-induced ACTH and corticosterone secretion

75%

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

Journal of Physiology and Pharmacology

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2001

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tom 52

|

nr 4,2

The involvement of prostaglandins synthesized by constitutive (COX-1) and inducible cyclooxygenase (COX-2) in central stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by adrenergic receptor agonists was investigated in conscious rats. COX-1 and COX-2 inhibitor, piroxicam (0.02 and 0.2 µg) and compound NS-398 (0.01 and 0.1 µg), respectively, were given intracerebroventricularly (i.c.v.) 15 min prior to i.c.v. adrenergic receptor agonists: phenylephrine (30 µg) and clonidine (10 µg), an alpha1- and alpha2-adrenergic agonist, and isoprenaline (20 µg) a non-selective ß-adrenergic agonist and clenbuterol (10 µg) a selective ß2-adrenergic agonist. Piroxicam and NS-398 considerably and dose-dependently reduced the phenylephrine-induced increase in ACTH and corticosterone secretion. Pretreatment with piroxicam and NS-398 markedly impaired the clonidine-evoked ACTH and corticosterone secretion. Piroxicam moderately diminished the isoprenaline-elicited increase in ACTH and corticosterone, while NS-398 did not markedly alter ACTH secretion. The clenbuterol-induced ACTH and corticosterone responses were considerably impaired by pretreatment with piroxicam, and slightly less potently by NS-398. These results indicate that in central structures involved in regulation of the HPA axis both constitutive and inducible cyclooxygenase are present under normal conditions in rats. These isoenzymes are significantly involved in the stimulatory signaling transduced by postsynaptic aalpha1-adrenergic receptors and, to a lesser extent, by a2-adrenergic receptors. Both isoenzymes affect moderately the stimulatory action of a non-selective ß-adrenergic agonist on ACTH and corticosterone secretion. COX-1 participates considerably and COX-2 markedly in the potent stimulatory action of selective ß2-adrenergic receptors on HPA axis.

8

The eicosanoid factor: a determinant of individuality of nephron segments

75%

McGiff J. C., Ferreri N. R., Carroll M. A.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,1

Nephron function is segmented; each segment has characteristic transport mechanisms and individual eicosanoid profiles. The transport function of the medullary thick ascending limb of Henle's loop (mTAL) establishes the osmolar gradient upon which extra cellular fluid volume (ECFV) conservation depends. The overriding importance of the mTAL to regulation of ECFV is evident in the diuretic- natriuretic potency of furosemide-like agents which target the mTAL. Results: The mTAL has been shown to be heavily invested with cytochrome P450 monooxygenases (CYP), chiefly / -1 hydroxylase activity, that generate 19- and 20-hydroxyeicosatetraenoic acid (HETEs). However, displacement of w hydroxylase by an inducible cyclooxygenase mechanism (COX-2) can be effected by several interventions: long-term infusion of angiotensin II (ANG II), adrenalectomy and elevated extracellular Ca2+ concentrations. This switching mechanism (CYP ³ COX- 2) has been shown to be dependent on activation of tumor necrosis factor alpha (TNFalpha) by ANG II. It represents a long-term adaptive mechanism of the mTAL with production of PGE2 whereas in the short-term, ANG II increases 20-HETE synthesis by the mTAL. The effect of Ca2+ on mTAL eicosanoid-related mechanisms provides an explanation for the natriuretic response to hypercalcemia and diminished ability to concentrate urine. Conclusion: The expression of COX-2 in the TAL has been linked to activation of the renin-angiotensin system, glucocorticoid deficiency and hypercalcemia, all of which operate through a mechanism in which production of TNFa by the TAL is pivotal.

9

Relation of adrenergic receptors, which have roles in gastroprotective and anti-inflammatory effect of adrenal gland hormones, with cyclooxygenase enzyme levels in rats

63%

Suleyman H., Dursun H., Bilici M., Cadirci E., Halici Z., Gulaboglu M., Albayrak F.

Journal of Physiology and Pharmacology

|

2009

|

tom 60

|

nr 4

129-134

Background and Aims: COX-2 enzyme inhibition is responsible for the anti-inflammatory effects of NSAIDs, COX-1 for their effects upon the gastrointestinal system (GIS), along with other side effects. We investigated the relationship between COX levels and those adrenergic receptors known to play a role in gastroprotection and anti-inflammatory activity. Method: The effects of adrenaline and prednisolone on gastric COX-1 and COX-2 levels in both intact and adrenalectomized rats treated with doxazosin, yohimbine, propranolol, and metoprolol were determined. Results: We found that adrenaline increases COX-1 levels in the gastric tissue of both intact and adrenalectomized rats by stimulating -2 receptors. Adrenaline decreases COX-2 levels by stimulating ß-2 adrenergic receptors. Prednisolone inhibits both COX-1 and COX-2 in the gastric tissue of intact rats. In adrenalectomized rats, prednisolone increases gastric COX-1 by stimulating -2 receptors, and decreases COX-2 levels by stimulating ß-2 receptors. Conclusion: Prednisolone cannot bind to a adrenergic receptors in the presence of adrenaline (intact rats) but, in its absence (adrenalectomy), binds to -2 receptors, and stimulates them more effectively than adrenaline, suggesting a direct relationship between -2 adrenergic receptors and COX-1 levels, whereas ß-2 receptors are directly related to COX-2 levels.

10

Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor

63%

Pytlowany M., Strosznajder J. B., Jesko H., Cakala M., Strosznajder R. P.

Acta Biochimica Polonica

|

2008

|

tom 55

|

nr 2

339-347

Nitric oxide (NO) is a potent extracellular and intracellular physiological messenger. However, NO liberated in excessive amounts can be involved in macromolecular and mitochondrial damage in brain aging and in neurodegenerative disorders. The molecular mechanism of its neurotoxic action is not fully understood. Our previous data indicated involvement of NO in the release of arachidonic acid (AA), a substrate for cyclo- and lipoxygenases (COX and LOX, respectively). In this study we investigated biochemical processes leading to cell death evoked by an NO donor, sodium nitroprusside (SNP). We found that SNP decreased viability of pheochromocytoma (PC12) cells in a concentration- and time-dependent manner. SNP at 0.1 mM caused a significant increase of apoptosis-inducing factor (AIF) protein level in mitochondria. Under these conditions 80% of PC12 cells survived. The enhancement of mitochondrial AIF level might protect most of PC12 cells against death. However, NO released from 0.5 mM SNP induced massive cell death but had no effect on protein level and localization of AIF and cytochrome c. Caspase-3 activity and poly(ADP-ribose) polymerase-1 (PARP-1) protein levels were not changed. However, PARP activity significantly decreased in a time-dependent manner. Inhibition of both COX isoforms and of 12/15-LOX significantly lowered the SNP-evoked cell death. We conclude that AIF, cytochrome cand caspase-3 are not responsible for the NO-mediated cell death evoked by SNP. The data demonstrate that NO liberated in excess decreases PARP-1 activity. Our results indicate that COX(s) and LOX(s) are involved in PC12 cell death evoked by NO released from its donor, SNP.

11

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Functional aspects of eicosanoid metabolism

63%

Carroll M. A., McGiff J. C.

Journal of Physiology and Pharmacology

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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.

12

The effect of resveratrol on contractility of non-pregnant rat uterus: the contribution of K+ channels

63%

Novakovic R., Ilic B., Beleslin-Cokic B., Radunovic N., Heinle H., Scepanovic R., Gojkovic-Bukarica L.

Journal of Physiology and Pharmacology

|

2013

|

tom 64

|

nr 6

13

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

63%

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

|

2013

|

tom 64

|

nr 5

14

Involvement of cyclooxygenase-1 and cyclooxygenase-2 activity in the therapeutic effect of ghrelin in the course of ethanol-induced gastric ulcers in rats

63%

Warzecha Z., Ceranowicz P., Dembinski M., Cieszkowski J., Ginter G., Ptak-Belowska A., Dembinski A.

Journal of Physiology and Pharmacology

|

2014

|

tom 65

|

nr 1

15

Anti-inflammatory effects of simvastatin in nonsteroidal anti-inflammatory drugs-induced small bowel injury

63%

Kim E. K., Cho J. H., Jeong A. R., Kim E. J., Park D. K., Kwon K. A., Chung J. W., Kim K. O., Kim J. H., Kim J. H., Kim Y. J.

Journal of Physiology and Pharmacology

|

2017

|

tom 68

|

nr 1

16

Vulnerability of gastric and small intestinal mucosa to ulcerogenic action of indomethacin in C57/BL6/J mice and transient receptor potential channel vanilloid type 1 knockout mice

63%

Yarushkina N. I., Sudalina M. N., Punin Y. M., Filaretova L. P.

Journal of Physiology and Pharmacology

|

2018

|

tom 69

|

nr 6

17

Prostaglandins and inflammation: the cyclooxygenase controversy

63%

Morteau O.

Archivum Immunologiae et Therapiae Experimentalis

|

2000

|

tom 48

|

nr 6 Spec.Iss.

473-480

18

The expression of COX-2, hTERT, MDM2, LATS2 and S100A2 in different types of non-small cell lung cancer [NSCLS]

63%

Strazisar M., Mlakar V., Glavac D.

Cellular and Molecular Biology Letters

|

2009

|

tom 14

|

nr 3

442-456

Several studies have reported different expression levels of certain genes in NSCLC, mostly related to the stage and advancement of the tumours. We investigated 65 stage I-III NSCLC tumours: 32 adenocarcinomas (ADC), 26 squamous cell carcinomas (SCC) and 7 large cell carcinomas (LCC). Using the real-time reverse transcription polymerase chain reaction (RT-PCR), we analysed the expression of the COX-2, hTERT, MDM2, LATS2 and S100A2 genes and researched the relationships between the NSCLC types and the differences in expression levels. The differences in the expression levels of the LATS2, S100A2 and hTERT genes in different types of NSCLC are significant. hTERT and COX-2 were over-expressed and LATS2 under-expressed in all NSCLC. We also detected significant relative differences in the expression of LATS2 and MDM2, hTERT and MDM2 in different types of NSCLC. There was a significant difference in the average expression levels in S100A2 for ADC and SCC. Our study shows differences in the expression patterns within the NSCLC group, which may mimic the expression of the individual NSCLC type, and also new relationships in the expression levels for different NSCLC types.

19

A downregulation of nNOS is associated to dysmotility evoked by lipopolysaccharide in rabbit duodenum

63%

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

Journal of Physiology and Pharmacology

|

2008

|

tom 59

|

nr 3

511-524

Alterations in gastrointestinal motility have been reported in response to endotoxin. The effects of lipopolysaccharide (LPS) on motility have been attributed to several substances, including prostaglandins and nitric oxide. The aim of this study was to investigate the expression and the contribution of NOS and COX enzymes to the local effect of LPS on ACh-evoked contractions in rabbit duodenum. The ACh evoked contractions were inhibited by LPS in longitudinal and circular muscles of duodenum. L-NNA, aminoguanidine, ODQ, indomethacin, and NS-398 but not NPLA antagonized the inhibitory effect of LPS. Western blot analysis showed protein bands of 155, 130, 70 and 72 kDa for nNOS, iNOS, COX-1 and COX-2 respectively in rabbit duodenum. All of these isoforms were expressed constitutively and only the nNOS was reduced in the presence of LPS. Expression of nNOS, iNOS, COX-1 and COX-2 was detected by inmunohistochemistry in the smooth muscle layers and in the neurons of the myenteric ganglia of rabbit duodenum. In conclusion, LPS locally administered reduces the contractility of rabbit duodenum and a downregulation of nNOS is associated to this effect. The iNOS, COX-1 and COX-2 were expressed constitutively but their expression was not modified by LPS.

20

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

63%

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

Journal of Physiology and Pharmacology

|

2014

|

tom 65

|

nr 1

Ograniczanie wyników

Tubular and vascular actions of cytochrome P450-arachidonate metabolites

Physiological mediators in nonsteroidal anti-inflammatory drugs (NSAIDs)-induced impairment of gastric mucosal defense and adaptation. Focus on nitric oxide and lipoxins

Cyclooxygenase pathways

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

Effects of indomethacin and rofecoxib on gastric mucosal damage in normal and Helicobacter pylori - infected Mongolian gerbils

Interleukin 1beta induces functional prostaglandin E synthase in cultured human umbilical vein endothelial cells

Involvement of constitutive (COX-1) and inducible cyclooxygenase (COX-2) in the adrenergic-induced ACTH and corticosterone secretion

The eicosanoid factor: a determinant of individuality of nephron segments

Relation of adrenergic receptors, which have roles in gastroprotective and anti-inflammatory effect of adrenal gland hormones, with cyclooxygenase enzyme levels in rats

Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor

Functional aspects of eicosanoid metabolism

The effect of resveratrol on contractility of non-pregnant rat uterus: the contribution of K+ channels

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

Involvement of cyclooxygenase-1 and cyclooxygenase-2 activity in the therapeutic effect of ghrelin in the course of ethanol-induced gastric ulcers in rats

Anti-inflammatory effects of simvastatin in nonsteroidal anti-inflammatory drugs-induced small bowel injury

Vulnerability of gastric and small intestinal mucosa to ulcerogenic action of indomethacin in C57/BL6/J mice and transient receptor potential channel vanilloid type 1 knockout mice

Prostaglandins and inflammation: the cyclooxygenase controversy