Wyniki wyszukiwania

1

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Inhibitory effects of indomethacin on growth and proliferation of gastric carcinoma cells Kato III

100%

Fujiwara Y., Tarnawski A., Fujiwara K., Arakawa T., Kobayashi K.

Journal of Physiology and Pharmacology

|

1993

|

tom 44

|

nr 2

2

Effects of sucralfate and its components on indomethacin-induced damage to cultured rabbit gastric mucosal cells

86%

Takahashi S., Okabe S.

Journal of Physiology and Pharmacology

|

1996

|

tom 47

|

nr 4

3

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

86%

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

Journal of Physiology and Pharmacology

|

2004

|

tom 55

|

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.

4

Effect and mechanism of sucralfate on healing of acetic acid-induced gastric ulcers in rats

86%

Ogihara Y., Okabe S.

Journal of Physiology and Pharmacology

|

1993

|

tom 44

|

nr 2

5

Urinary gamma-glutamyl transferase activity in rats with nonsteroidal anti-inflammatory drug-induced nephrotoxicity

86%

Kocaoglu S., Karan A., Berkan T., Basdemir G., Akpinar R.

Archivum Immunologiae et Therapiae Experimentalis

|

1997

|

tom 45

|

nr 1

6

The influence of indomethacin on the ACTH secretion induced by central stimulation of adrenergic receptors

86%

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

Journal of Physiology and Pharmacology

|

2000

|

tom 51

|

nr 2

7

Oenothera paradoxa defatted seeds extract containing pentagalloylglucose and procyanidins potentiates the cytotoxicity of vincristine

72%

Jaszewska E., Kosmider A., Kiss A. K., Naruszewicz M.

Journal of Physiology and Pharmacology

|

2010

|

tom 61

|

nr 5

8

Comparison of prostaglandin and cimetidine in protection of isolated gastric glands against indomethacin injury

72%

Brzozowski T., Tarnawski A., Hollander D., Sekhon S., Krause W. J., Gergely H.

Journal of Physiology and Pharmacology. Supplement

|

2005

|

tom 56

|

nr 5

75-88

Prostaglandins can protect the in vivo gastric mucosa against necrosis produced by a variety noxious agents. Cimetidine has also been shown to have protective properties in humans and in some models of experimental injury. Whether prostaglandins or cimetidine may protect gastric mucosal cells directly in the absence of systemic factors remains controversial. In the present study, the potential protective actions of prostaglandin and cimetidine against indomethacin injury were assessed in isolated rat gastric glands. Gastric glands were pre-incubated in oxygenated medium with either placebo, 16,16 dimethyl prostaglandin E2 (dm PGE2) or cimetidine and incubated at 37°C in medium containing 0.5 mg/ml of indomethacin for 2, 4 and 6 hrs. Cell injury and protection was assessed by the Fast Green exclusion test (viability test), leakage of lactate dehydrogenase (LDH) into the medium, and by scanning and transmission electron microscopy. In addition, the generation of PGE2 by the gland cells was determined using RIA assay. Indomethacin by itself significantly reduced the viability of gastric glands, increased LDH release into the medium and produced prominent ultrastructural damage. In contrast to cimetidine, co-incubation of gastric glands with dm PGE2 added to indomethacin, significantly reduced indomethacin-induced injury, increased the number of viable cells, reduced LDH leakage and diminished the extent of ultrastructural damage. The dose of indomethacin (5 µg/ml) which significantly inhibited the generation of PGE2 (up to 90% inhibition) had no effect on cell viability nor LDH release. We conclude that 1) exogenous PGE2 exerts a potent protective activity in vitro which is independent on neural, vascular and hormonal factors; 2) inhibition of endogenous PGs may not the primary mechanism in the deleterious action of indomethacin against damage to gastric glandular cells and 3) indomethacin can exert a direct cytotoxic effect on the mucosal cells in gastric glands.

9

Influence of forced treadmill and voluntary wheel running on the sensitivity of gastric mucosa to ulcerogenic stimuli in male rats

72%

Yarushkina N. I., Komkova O. P., Filaretova L. P.

Journal of Physiology and Pharmacology

|

2020

|

tom 71

|

nr 6

10

Assessment of neurotoxicity of pharmacological compounds during early neural development of human embryonic stem cells

72%

Kang H. Y., Hong E. J., Kang H. S., Ahn C., Jeung E. B.

Journal of Physiology and Pharmacology

|

2017

|

tom 68

|

nr 2

11

Effects of stress preconditioning on vulnerability of gastric and small intestinal mucosa to ulcerogenic action of indomethacin in rats

72%

Yarushkina N. I., Filaretova L. P.

Journal of Physiology and Pharmacology

|

2019

|

tom 70

|

nr 6

12

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

72%

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

Journal of Physiology and Pharmacology

|

2018

|

tom 69

|

nr 6

13

Leukotrienes in mucosal damage and protection

72%

Peskar B. M.

Journal of Physiology and Pharmacology

|

1991

|

tom 42

|

nr 2

Exposure of the rat gastric mucosa to ethanol stimulates the generation of leukotriene (LTC₄) and 15-hydroxyeicosatetraenoic acid, hut not of thromboxanes and prostaglandins. Lipoxygenase activation is not found with other topical irritants or nonsteroidal anti-inflammatory drugs. A number of gastroprotective drugs dose-dependently inhibit the stimulatory action of ethanol on mucosal LTC₄ formation closely parallel to their protective activity suggesting that ethanol-induced damage and activation of lipoxygenases may involve common targets which are simultaneously counteracted by certain types of protective agents. Selective inhibition of 5-lip- oxygenase, however, does not confer protection against gastric mucosal damage caused by topical irritants or non-steroidal anti-inflammatory drugs. Thus, although leukotrienes may mediate certain reactions elicited by gastric ulcerogens such as submucosal venular constriction and mucosal micro vascular engorgement, they do not appear to be major mediators of ulcerogen-induced tissue necrosis. The contribution of other products of the various pathways of arachidonic acid metabolism to gastric mucosal injury and the mechanism underlying the close interrelationship between protection and inhibiton of LTC₄ formation observed with certain compounds remains to be investigated.

14

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

72%

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

Journal of Physiology and Pharmacology. Supplement

|

2003

|

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.

15

Role of prostaglandins in heme-induced fever

72%

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

Journal of Physiology and Pharmacology. Supplement

|

2006

|

tom 57

|

nr 8

73-82

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.

16

The effects of indomethacin on angiogenic factors mRNA expression in renal cortex of healthy rats

72%

Mucha K., Foroncewicz B., Koziak K., Czarkowska-Paczek B., Paczek L.

Journal of Physiology and Pharmacology

|

2007

|

tom 58

|

nr 1

Indomethacin is a nonsteroidal anti-inflammatory drug used frequently to control chronic or temporary pain. In the kidney, indomethacin decreases medullary and cortical perfusion, resulting in hypoxia. Kidney hypoxia has many effects, including changes in gene expression, and is a strong stimulus for angiogenesis. Other angiogenic factors include vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2), transforming growth factor beta 1 (TGFß1), and platelet-derived growth factor (PDGF). Our goal was to examine the influence of indomethacin on mRNA expression of these factors and their selected receptors in the renal cortex of healthy rats. Groups of 8 healthy, male, six-week-old Wistar rats received either indomethacin (5 mg/kg/day) or placebo orally for three months. RNA from renal cortex biopsies was analyzed by real-time polymerase chain reaction to quantify the mRNA levels of each cytokine. We observed significantly higher mRNA levels for VEGF (1.73-fold), FGF-2 (5.6-fold) and TGFß receptor III (2.93-fold), PDGF receptor alpha (2.93-fold) and receptor ß (2.91-fold) in rats receiving indomethacin compared to rats given placebo (p < 0.05). Amounts of mRNA for TGFß1, PDGF, FGF receptors 1 and 2 and TGFß receptor I did not differ between analysed groups. Our data indicates that indomethacin may regulate the expression of potent angiogenic factors VEGF and FGF-2.

17

Involvement of cyclooxygenase-derived prostaglandin E2 and nitric oxide in the protection of rat pancreas afforded by low dose of lipopolysaccharide

72%

Jaworek J., Bonior J., Tomaszewska R., Jachimczak B., Kot M., Bielanski W., Pawlik W. W., Sendur R., Stachura J., Konturek P. C., Konturek S. J.

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 1

18

Endothelial secretogogues and deformability of erythrocytes

72%

Korbut R. A., Adamek-Guzik T., Madej J., Korbut R.

Journal of Physiology and Pharmacology

|

2002

|

tom 53

|

nr 4,1

Many diseases of the heart and circulatory system have been linked with both dysfunction of vascular endothelium and insufficient deformability of erythrocytes. Using shear stress laser diffractometry we investigated whether deformability of erythrocytes would be regulated endogenously by generation of two endothelial secretogogues: prostacyclin and nitric oxide. Experiments were performed in rats ex vivo and with whole blood or isolated erythrocytes in vitro. Iloprost - a stable analogue of prostacyclin (10 µg/kg i.v.) and SIN-1 (NO-donor) at a dose of 2 mg/kg/min i.v induced a significant improvement of deformability of erythrocytes ex vivo. Improvements of deformability by these two compounds were also evident in vitro when they were applied at a range of concentrations of 1 µM and 3 µM, respectively. Cyclooxygenase (indomethacin 20 mg.kg i.v.) and nitric oxide synthase (L-NAME 10 mg/kg i.v.) inhibitors while worsening deformability ex vivo, they did not affect (3 mM and 10 µM, respectively) rheological functions of erythocytes in vitro. Aggravating effects of these inhibitors on erythrocyte deformability ex vivo were reversed by prostacyclin and nitric oxide supplemented exogenously. Aspirin at a low (1 mg/kg i.v.) and high dose (50 mg/kg i.v.), contrary to indomethacin and L- NAME, aggravated erythrocyte deformability either ex vivo or in vitro. It is concluded that autocrine function of vascular endothelium plays an important role in regulation of rheology of red blood cells in flowing blood. The mechanism of this phenomenon is unclear but some possible explanations are discussed. In addition, in our experiments aspirin revealed unique erythrocyte damaging properties, possibly independent of inhibition of cyclooxygenase, but related to a direct protein acetylation.

19

Involvement of heat shock proteins in the healing of acetic acid-induced gastric ulcers in rats

72%

Tsukimi Y., Nakai H., Itoh S., Amagase K., Okabe S.

Journal of Physiology and Pharmacology

|

2001

|

tom 52

|

nr 3

20

Direct protective action of epidermal growth factor on isolated gastric mucosal surface epithelial cells

72%

Ishikawa T., Fukuda T., Sugiyama M., Tarnawski A.

Journal of Physiology and Pharmacology

|

1992

|

tom 43

|

nr 4

Epidermal growth factor (EGF) protects gastric mucosa against acute injury produced by a variety of damaging agents, but the mechanism of its protective action is not clear. Since the surface epithelial cells (SEC) are important component of gastric mucosal defence, we studied whether EGF may directly protect isolated gastric SEC against ethanol injury in vitro, in condition independent of systemic factors and whether endogenous prostaglandins may play a role in EGF’s protective action. The isolated SEC from rat gastric mucosa were preincubated in medium only, or medium containing 0.0001-10.0 µg/ml of h-rEGF for 15 minutes, and incubated with 8% ethanol for 1 hour. In another study the above experiment was repeated but cells were pretreated with 10⁻⁴ or 10⁻⁵ M indomethacin before EGF treatment. The cell viability was assessed by fast green exclusion test. Incubation of SEC with 8% ethanol significantly reduced SEC cell viability to 50 ₋⁺ 2%: EGF 0.1 or 1.0/µg/ml significantly reduced ethanol induced damage (cell viability 59 ₋⁺ 3 and 62₋⁺ 3% respectively). Pretreatment with 10⁻⁴ M indomethacin (the dose which does not affect SEC viability but inhibit PGE₂ and PGI₂ generation), significantly reduced protective action of EGF against 8% ethanol injury. EGF 1.0 and 10.0 µg/ml alone without ethanol increased PGE₂ and 6 keto PGF₁α generation by SEC. These studies demonstrated: 1) EGF is able to protect gastric surface epithelial cells directly without mediation by systemic factors. 2) EGF induced protection of SEC may in part be mediated by prostaglandins.

Ograniczanie wyników

Inhibitory effects of indomethacin on growth and proliferation of gastric carcinoma cells Kato III

Effects of sucralfate and its components on indomethacin-induced damage to cultured rabbit gastric mucosal cells

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

Effect and mechanism of sucralfate on healing of acetic acid-induced gastric ulcers in rats

Urinary gamma-glutamyl transferase activity in rats with nonsteroidal anti-inflammatory drug-induced nephrotoxicity

The influence of indomethacin on the ACTH secretion induced by central stimulation of adrenergic receptors

Oenothera paradoxa defatted seeds extract containing pentagalloylglucose and procyanidins potentiates the cytotoxicity of vincristine

Comparison of prostaglandin and cimetidine in protection of isolated gastric glands against indomethacin injury

Influence of forced treadmill and voluntary wheel running on the sensitivity of gastric mucosa to ulcerogenic stimuli in male rats

Assessment of neurotoxicity of pharmacological compounds during early neural development of human embryonic stem cells

Effects of stress preconditioning on vulnerability of gastric and small intestinal mucosa to ulcerogenic action of indomethacin in rats

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

Leukotrienes in mucosal damage and protection

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

Role of prostaglandins in heme-induced fever

The effects of indomethacin on angiogenic factors mRNA expression in renal cortex of healthy rats