Wyniki wyszukiwania - Biblioteka Nauki

1

Role of the p38 MAPK pathway in induction of iNOS expression in human leukocytes

100%

Jablonska E. , Ratajczak W. , Jablonski J.

Folia Biologica

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2008

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tom 56

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nr 1-2

83-89

2

Effects of IFN-beta1a and IFN-beta1b treatment on the expression of cytokines, inducible NOS (NOS type II), and myelin proteins in animal model of multiple sclerosis

84%

Lubina-Dabrowska N. , Stepien A. , Sulkowski G. , Dabrowska-Bouta B. , Langfort J. , Chalimoniuk M.

Archivum Immunologiae et Therapiae Experimentalis

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2017

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tom 65

|

nr 4

3

Blockade of nitric oxide formation in the rat brain does not disturb development of endotoxin tolerance

84%

Soszynski D. , Daniluk M. , Galazka M. , Dmitruk K.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 6

4

ST36 electroacupuncture activates nNOS, iNOS and ATP-sensitive potassium channels to promote orofacial antinociception in rats

84%

Almeida R. T. , Galdino G. , Perez A. C. , Silva G. , Romero T. R. , Duarte I. D.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 1

5

Immunohistochemical visualization of pro-inflammatory cytokines and enzymes in ovarian tumors

84%

Plewka D. , Kowalczyk A. E. , Jakubiec-Bartnik B. , Morek M. , Bogunia E. , Kmiec A. , Wierzbicki P. M. , Plewka A.

Folia Histochemica et Cytobiologica

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2014

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tom 52

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nr 2

6

Ascorbic acid attenuates aspirin-induced gastric damage: role of inducible nitric oxide synthase

84%

Konturek P. C. , Kania J. , Hahn E. G. , Konturek J. W.

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tom 57

|

nr 5

125-136

EN

Aspirin (ASA) represents an important risk factor for gastric mucosal injury. Recently, vitamin C releasing aspirin (ASA-VitC) has been shown to reduce gastric toxicity of ASA in animal model of gastric injury. The aim of the present study was to compare the effect of ASA and ASA-VitC on the gastric mucosal damage before and after Helicobacter pylori (Hp) eradication in 10 young healthy Hp-positive volunteers. All subjects underwent endoscopy at day 0 (before ASA or ASA-VitC treatment) and at day 3 following treatment (1.6 g ASA/day or 1.6 g ASA + 0.96 g Vit C/day). In addition, in vitro experiments were performed in which gastric mucosal cell line (MKN-45 cells) was incubated with ASA or ASA-VitC alone or in combination with H.pylori. Expression of constitutive and inducible NO synthase (cNOS, iNOS) was analyzed by Western blot. Moreover, COX-2 expression was analyzed in gastric biopsies at mRNA and protein level by RT-PCR and Western blot, repectively. In humans, treatment with ASA-VitC induced significantly less gastric mucosal lesions than plain ASA. Furthermore, in comparision to plain ASA, ASA-VitC caused stronger inhibition of cNOS and increase in iNOS expression in the gastric mucosa. in vitro studies demonstrated a significant increase in iNOS expression in MKN-45 cells incubated with Hp. This effect was aggravated by the addition of ASA, but not ASA-VitC, to MKN-45 cells incubated with H.pylori. Both ASA and ASA-VitC stimulated the COX-2 expression in the gastric mucosa. We conclude that ASA-VitC in comparison with ASA induces less gastric mucosal damage and this protective effect may be due to its inhibitory effect on iNOS expression.

7

The effect of Naja naja oxiana snake venom against Leishmania tropica confirmed by advanced assays

84%

Sharifi I. , Tabatabaie F. , Nikpour S. , Mostafavi M. , Oliaee R. T. , Sharifi F. , Babaei Z. , Jafari E. , Salarkia E. , Shahbazzadeh D.

Acta Parasitologica

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2021

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tom 66

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nr 2

8

Role of endothelial nitric oxide synthase in aggravation of indomethacin-induced gastric damage in adjuvant arthritic rats

84%

Kato S. , Ohkawa F. , Ito Y. , Amagase K. , Takeuchi K.

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nr 4

147-155

EN

The role of nitric oxide synthase (NOS) isozymes in the aggravation of indomethacin-induced gastric damage in adjuvant arthritic rats was investigated. Two weeks after injection of Freund’s complete adjuvant, the animals were given indomethacin, and the stomach was examined for damage 4 h later. Indomethacin caused hemorrhagic lesions in the normal rat stomach, and these lesions were markedly aggravated in arthritic rats. Pretreatment with L-NAME (a nonselective inhibitor of NOS) and aminoguanidine (a relative selective inhibitor of iNOS) did not affect the ulcerogenic response in normal rats but dose-dependently prevented the aggravation of lesions in arthritic rats, but the effect of aminoguanidine was apparently less than that of L-NAME. The increased ulcerogenic response in arthritic rats was significantly suppressed by 1400 W (a selective inhibitor of iNOS) and L-NIO (a selective inhibitor of eNOS) but not by L-NPA (a selective inhibitor of nNOS). The concurrent administration of 1400 W and L-NIO almost totally abolished the aggravation of damage in arthritic rats. The expressions of eNOS and iNOS but not nNOS in the gastric mucosa were clearly enhanced in arthritic rats. Mucosal levels of non-protein sulfhydryls were significantly lower in arthritic rats than those in normal rats. The aggravation of damage in arthritic rats was significantly prevented by glutathione. These results suggest that the increased ulcerogenic response to indomethacin in arthritic rat stomachs is mediated by NO derived from eNOS in addition to iNOS. It is assumed that eNOS/NO may act harmfully on the gastric mucosa of arthritic rats with mucosal SH deficiency.

9

Neuroprotective effect of resveratrol against late cerebral ischemia reperfusion induced oxidative stress damage involves upregulation of osteopontin and inhibition of interleukin-1beta

84%

Al Dera H.

Journal of Physiology and Pharmacology

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2017

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tom 68

|

nr 1

10

Cinacalcet, a calcimimetic, prevents nonsteroidal antiinflammatory drug-induced small intestinal damage in rats

84%

Hayashi S. , Kurata N. , Kitahirachi E. , Nishimura Y. , Amagase K. , Yano T. , Takeuchi K.

Journal of Physiology and Pharmacology

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2013

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tom 64

|

nr 4

11

Japanese quince (Chaenomeles japonica) leaf phenol extract as modulator of the inflammatory response in lipopolysaccharide-triggered murine macrophage RAW 264.7 cells

84%

Chojnacka K. , Owczarek K. , Caban M. , Sosnowska D. , Polka D. , Koziolkiewicz M. , Fichna J. , Lewandowska U.

Journal of Physiology and Pharmacology

|

2020

|

tom 71

|

nr 6

12

Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors does not influence febrile response in rats during turpentine abscess

84%

Soszynski D. , Chelminiak M.

Journal of Physiology and Pharmacology

|

2007

|

tom 58

|

nr 4

EN

The purpose of this study was to investigate the role of neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS) in the brain during development of fever in response to localized tissue inflammation caused by injection of turpentine in freely moving biotelemetered rats. To determine the role of both NOSs in turpentine-induced fever, we injected vinyl-L-NIO (N5 – (1-Imino-3-butenyl) – ornithine (vL-NIO), a selective nNOS inhibitor, and aminoguanidine hydrochloride, a selective iNOS inhibitor, intracerebroventricularly (i.c.v.) 5 h after turpentine injection. Rats responded with fever to intramuscular injection of 20 µl of turpentine that commenced about 5 - 6 h after injection and reached peak value between 9 - 11 h post-turpentine. The inhibition of nNOS as well as iNOS in the brain did not affect fever induced by turpentine. Fevers in control rats (treated i.c.v. with pyrogen-free water) and iNOS or nNOS inhibitor-i.c.v. treated rats injected with turpentine were essentially the same. Furthermore, on the basis of these data, we concluded that iNOS and nNOS inside the brain do not participate in generation of fever to turpentine in rats.

13

Beta-carotene inhibits Helicobacter pylori-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 in human gastric epithelial AGS cells

67%

Jang S. H. , Lim J. W. , Kim H.

|

tom 60

|

nr 7

14

Metallothioneins in the lung cancer

67%

Werynska B. , Pula B. , Kobierzycki C. , Dziegiel P. , Podhorska-Okolow M.

Folia Histochemica et Cytobiologica

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2015

|

tom 53

|

nr 1

15

Pathological study of chronic pulmonary toxicity induced by intratracheally instilled Asian sand dust (Kosa): possible association of fibrosis with the development of granulomatous lesions

67%

Shimada A. , Kohara Y. , Naota M. , Kobayashi Y. , Morita T. , Inoue K. , Takano H.

Folia Histochemica et Cytobiologica

|

2015

|

tom 53

|

nr 4

16

Melatonin in gastroprotection against stress-induced acute gastric lesions and in healing of chronic gastric ulcers

67%

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

|

tom 57

|

nr 5

51-66

EN

The degree of gastric damage following to exposition of the mucosa to noxious agents depends upon a balance between the factors promoting this damage and those activating the natural defense mechanisms. Recent findings, presented in this review, provide evidence that melatonin prevents the formation of acute gastric lesions induced by stress and accelerates healing of chronic gastric ulcers due to increase in the activity of nitric oxide (NO) synthase (NOS)-NO and cyclooxygenase (COX)-prostaglandin E2 (PGE2) systems resulting in the increase of mucosal blood flow and mucosal integrity. Melatonin is produced and released into the circulation by the pineal gland and, in many times larger amounts, by the gastrointestinal tract. Due to its anti-inflammatory and anti-oxidant properties, melatonin may be one of the most efficient protective factors preventing the development of acute gastric damage and accelerating healing of chronic gastric ulcers probably due to reduction in proinflammatory cytokine production, scavenging of the radical oxygen species and activation of COX-PG and NOS-NO systems as well as stimulating the afferent sensory nerves in the brain-gut axis.

17

Human umbilical cord expresses several vasoactive peptides involved in the local regulation of vascular tone: protein and gene expression of Orphanin, Oxytocin, ANP, eNOS and iNOS

67%

Mauro A. , Buscemi M. , Provenzano S. , Gerbino A.

Folia Histochemica et Cytobiologica

|

2011

|

tom 49

|

nr 2

18

Spent hops (Humulus lupulus L.) extract as modulator of the inflammatory response in lipopolysaccharide stimulated raw 264.7 macrophage

67%

Caban M. , Chojnacka K. , Owczarek K. , Laskowska J. , Fichna J. , Podsedek A. , Sosnowska D. , Lewandowska U.

Journal of Physiology and Pharmacology

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2020

|

tom 71

|

nr 1

19

Nitric oxide-induced IL-8 expression is mediated by NF-kappaB and AP-1 in gastric epithelial AGS cells

67%

Seo J. Y. , Ju J.-H. , Lim J. W. , Mukaida N. , Kim H.

|

tom 60

|

nr 7

20

Molecular mechanism of emotional fever - the role of nitric oxide

67%

Soszynski D.

|

nr 8

51-59

EN

The purpose of these studies was to assess the involvement of nNOS and iNOS inhibitors on stress fever caused by exposure to an open field in freely moving biotelemetered rats. Vinyl-L-NIO (N5 - (1-Imino-3-butenyl) - ornithine, a neural nitric oxide synthase (nNOS) inhibitor, and aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, were injected into the lateral ventricle (icv) at a dose of 5 µg and 10 µg, respectively, and then immediately exposed to open field for 30 min. After exposure to the open field, rats not treated with NOS inhibitors responded with a rapid rise in Tb and it was accompanied with an increase of motor activity. Both inhibitors significantly suppressed the stress fever. vL-NIO did not influence stress-induced rise in locomotor activity as well as did not change Tb in unstressed rats. Since aminoguanidine caused a transient fall in Tb below the baseline in rats exposed or not to open field and because this inhibitor suppressed stress-induced rise in locomotor activity, we concluded that nNOS expression inside the brain is critically involved in the rise in Tb due to exposure to psychological stress.