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  1. 26 Journal of Physiology and Pharmacology

  2. 13 Journal of Physiology and Pharmacology. Supplement

  3. 4 Archivum Immunologiae et Therapiae Experimentalis

  4. 1 Folia Biologica

  5. 1 Folia Histochemica et Cytobiologica

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  1. 6 Brzozowski T.

  2. 5 Takeuchi K.

  3. 4 Konturek P. C.

  4. 4 Konturek S. J.

  5. 4 Pawlik W. W.

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  1. 2 2021

  2. 1 2019

  3. 2 2018

  4. 4 2017

  5. 1 2014

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1
Content available remote

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

100%
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
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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.
2
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Significance of salicylate intolerance in diseases of the lower gastrointestinal tract

86%
Raithel M., Baenkler H. W., Naegel A., Buchwald F., Schultis H. W., Backhaus B., Kimpel S., Koch H., Mach K., Hahn E. G., Konturek P. C.
Journal of Physiology and Pharmacology. Supplement
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2005
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tom 56
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nr 5
89-102
Salicylate intolerance is defined as a nonspecific antigen-induced pseudo-allergic hypersensitivity reaction which can occur upon contact of an organism with salicylic acid, its derivatives or other related organic or inorganic acids of similar chemical structure. Since the effects of nonsteroidal anti-inflammatory drugs (NSAID) intolerance are by no means always severe or life-endangering but may just as well present as oligosymptomatic or local disorders (e.g. abdominal pain, diarrhea, we decided to evaluate the characteristics of patients with salicylate intolerance on the basis of gastroenterological case material of Medical Department I of Erlangen University. On the basis of the findings from the Erlangen interdisciplinary data register of chronic inflammatory gastrointestinal disease, the signs and symptoms of NSAID intolerance were found to constitute a diagnosis of great practical import to clinical medicine (allergology, dermatology, immunology, other disorders etc.) including gastroenterology. For approx. 2-7% of all patients with inflammatory bowel syndrome and food allergies this poses a new diagnostic and therapeutic challenge which may concern physicians from any of the disciplines involved. When presented with patients with chronic active disease who are suffering from these symptoms one should, therefore, in future give greater thought to the possibility of salicylate intolerance, all the more as there are meaningful dietetic, diagnostic and therapeutic options available for these persons.
3
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Discovery by Jaworski of Helicobacter pylori and its pathogenetic role in peptic ulcer, gastritis and gastric cancer

86%
Konturek J. W.
Journal of Physiology and Pharmacology. Supplement
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2003
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tom 54
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nr 3
23-41
The presence of spiral-shaped micro-organisms in the human stomach was described over 100 years ago by Polish clinical researcher, Professor W. Jaworski at Cracow Jagiellonian University. Their presence was then confirmed in animals by G. Bizzazero, but was not really taken seriously until the late 1970s, when J.R. Warren, a pathologist in Perth, Australia, noted the appearance of spiral bacteria overlaying gastric mucosa, chiefly over inflamed tissue. Warren and B.J. Marshall cultured these organisms in 1982 from 11 patients with gastritis and were able to demonstrate a strong association between the presence of Helicobacter pylori (H. pylori) and the finding of inflammation in gastric biopsies. People, who did not exhibit gastritis, also did not have the organism, a finding which was confirmed in a number of studies. Originally called Campylobacter pyloridis, the name was changed to Campylobacter pylori, and then later to Helicobacter pylori (H. pylori) as specific morphologic, structural, and genetic features indicated that it should be placed in a new genus. Marshall elegantly fulfilled Koch's postulates for the role of H. pylori in antral gastritis with the self administration of H. pylori, and also showed that it could be cured by use of antibiotics and bismuth salts. Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however, H. pylori causes chronic active, chronic persistent, and atrophic gastritis in adults and children. Infection with H. pylori also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts. The role of H. pylori in non-ulcer dyspepsia remains unclear. These practical aspects of H. pylori were subjects of two international symposia organized by us in 1995 and 1997 in Cracow, helping to promote research and Polish consensus regarding treatment of H. pylori infection.
4

Influence of nonsteroidal anti-inflammatory drugs on progesterone production by cultured bovine luteal cells

86%
Jaroszewski J. J., Markiewicz W., Maslanka T. S., Skarzynski D. J.
Polish Journal of Veterinary Sciences
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2009
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tom 12
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nr 3
The objective of the present study was to determine the influence of nonsteroidal anti-inflammatory drugs (NSAIDs) representing different chemical groups on progesterone (P₄) production by cultured bovine steroidogenic luteal cells. The cells were enzymatically isolated from corpora lutea collected on days 8-12 of the estrous cycle. After 24 h preincubation they were incubated for 24 h with medium only (control) or stimulated with bovine luteinizing hormone – LH (100 ng/ml; positive control) or increasing concentrations (10⁻⁸ to 10⁻⁴ M) of acetylsalicylic acid, indomethacin, ibuprofen, naproxen, piroxicam, phenylbutazone, dipyrone or nimesulide. Concentartions of P₄ in the culture media were determined by enzyme immunoassay. LH significantly increased P₄ secretion, while acetylsalicylic acid and indomethacin did not affect the production of this hormone. A significant increase in P₄ secretion was observed after administration of dipyrone at all concentrations, piroxicam at concentrations of 10⁻⁸, 10⁻⁷ and 10⁻⁵ M, phenylbutazone and naproxen at concentrations of 10⁻⁷ and 10⁻⁶ M and ibuprofen at concentrations of 10⁻⁵ and 10⁻⁴ M. Nimesulide did not affect P₄ production at concentrations of 10⁻⁸ – 10⁻⁵ M, while at a concentration of 10⁻⁴ M it inhibited P₄ secretion. The results obtained indicate that NSAIDs may change the production of P₄ in bovine luteal cells, however, these changes are dependent on the substance used.
5
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The essential oil from Ferulago angulata (Schltdl.) Boiss. fruits exerting potent analgesic and anti-inflammatory effects

86%
Shafaroodi H., Roozbahani S., Asgarpanah J.
Journal of Physiology and Pharmacology
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2021
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tom 72
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nr 1
6
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Cardiovascular and gastrointestinal toxicity of selective cyclo-oxygenase-2 inhibitors in man

86%
Dajani E. Z., Islam K.
Journal of Physiology and Pharmacology. Supplement
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2008
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tom 59
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nr 2
It is well established that the use of traditional nonsteroidal anti-inflammatory drugs (NSAIDs) increase the vulnerability of the gastrointestinal (GI) mucosa for the development of peptic lesions and serious ulcer complications. In addition, selective and traditional NSAIDs have also been associated with increased frequency of cardiovascular toxicity, especially in susceptible patients. The objective of this communication is to provide an overview of the salient GI and cardiovascular (CV) toxicity for these drugs. Traditional NSAIDs inhibit the constitutional cyclooxygenase-1 (COX-1) enzyme responsible for eicosanoids biosynthesis not only in joints, a beneficial effect, but also in the stomach, a detrimental effect. Selective NSAIDs were specifically designed to preferentially inhibit the cyclooxygenase-2 (COX-2), an inducible enzyme mediating the production of inflammatory eicosanoids in the joints but sparing the endogenous protective eicosanoids in the stomach. Selective COX-2 inhibitors (COXIBs) have been shown to possess much improved GI tolerability and reduced GI related adverse events when compared with nonselective COX-1inhibitors. An unexpected CV toxicity had emerged during the COXIBs post marketing outcome studies. Many subsequent studies were carried out to define the CV risks associated with COXIBs and NSAIDs. All COX inhibitors had shown this CV toxicity. In many clinical studies, rofecoxib use was associated with significantly more elevated CV risk when compared with celecoxib and non selective NSAIDs. The COX inhibitors associated CV toxicity has multiple manifestations, which include the induction of myocardial infarction (MI), edema, thrombosis, blood pressure destabilization and death. Patients at risk of CV disease or with a history of CV disease were the most significant determinants of CV events after receiving COX inhibitors. This CV toxicity not only led to the marketing withdrawal of rofecoxib and valdecoxib but also resulted in more restricted, but essentially identical, product labels in the United States for celecoxib and traditional NSAIDS. This CV toxicity is dose and treatment duration dependent and appears to be compound specific rather than COX specific. Additional comprehensive, long-term, prospective investigations comparing the CV and GI safety profile of marketed NSAIDs against each other and against selective inhibitors are needed to address the controversy of COX inhibitors.
7
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Content available

Delay in oral mucosal ulcer healing by aspirin is linked to the disturbances in p38 mitogen-activated protein kinase activation

86%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
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2001
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tom 52
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nr 2
8

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
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1997
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tom 45
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nr 1
9
Content available remote

Stable gastric pentadecapeptide BPC 157 heals cysteamine-colitis and colon-colon-anastomosis and counteracts cuprizone brain injuries and motor disability

72%
Klicek R., Kolenc D., Suran J., Drmic D., Brcic L., Aralica G., Sever M., Holjevac J., Radic B., Turudic T., Kokot A., Patrij L., Rucman R., Seiwerth S., Sikiric P.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 5
10
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The effect of resveratrol on contractility of non-pregnant rat uterus: the contribution of K+ channels

72%
Novakovic R., Ilic B., Beleslin-Cokic B., Radunovic N., Heinle H., Scepanovic R., Gojkovic-Bukarica L.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 6
11
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Prophylactic effect of egualen sodium, a stable azulene derivative, on gastrointestinal damage induced by ischemia-reperfusion, double antiplatelet therapy and loxoprofen in rats

72%
Amagase K., Yoshida Y., Hara D., Murakami T., Takeuchi K.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 1
12
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The effect of hydrogen sulfide-releasing naproxen (ATB-346) versus naproxen on formation of stress-induced gastric lesions. The regulation of systemic inflammation, hypoxia and alterations in gastric microcirculation

72%
Magierowski M., Magierowska K., Surmiak M., Hubalewska-Mazgaj M., Kwiecien S., Wallace J. L., Brzozowski T.
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 5
13
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Anti-inflammatory effects of simvastatin in nonsteroidal anti-inflammatory drugs-induced small bowel injury

72%
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
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2017
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tom 68
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nr 1
14
Content available remote

Underlying mechanism of regulatory actions of diclofenac, a nonsteroidal anti-inflammatory agent, on neuronal potassium channels and firing: an experimental and theoretical study

72%
Huang C. W., Hung T. Y., Liao Y. K., Hsu M. C., Wu S. N.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 3
15

Changes of interleukin-1beta and testosterone concentration after nonsteroidal anti-inflammatory drug treatment at different times relative to endotoxin administration in an equine model

72%
Danek J., Krumrych W., Golda R.
Folia Biologica
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2017
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tom 65
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nr 2
16
Content available remote

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

72%
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
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nr 4
17

Effects of selected nonsteroidal anti-inflammatory drugs on acute-phase protein levels after dehorning in Holstein heifers

72%
Erdogan H., Akin I., Ural K., Ulutas P. A.
Medycyna Weterynaryjna
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2019
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tom 75
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nr 07
The purpose of this study was to evaluate the effects of ketoprofen (KTP), flunixin meglumine (FLM), and meloxicam (MLX) administration on acute-phase proteins after dehorning in Holstein heifers. A total of 21 Holstein heifers were enrolled into three groups of equal size (n=7) and administered ketoprofen, flunixin meglumine, or meloxicam, at doses of 2.2 mg/kg, 1.1 mg/kg, and 1 mg/kg body weight, respectively. Serum amyloid A, haptoglobin, and ceruloplasmin levels were determined before the administration of the three drugs (0 hrs) and at 6, 12, 24, 48, and 96 hours post-administration. The mean values (±SD) obtained revealed no significant alteration in APP levels at 0 hrs in any of the three groups. Time-dependent alterations, however, were significant in all groups. Group-time interactions were significant (P < 0.001) for ceruloplasmin concentrations, whereas results for serum amyloid A and haptoglobin levels were deemed non-significant. Inter-group interaction revealed no significant findings regarding serum amyloid A and ceruloplasmin levels, but haptoglobin levels showed a significant difference between the KTP and FLM groups at 48 hrs. It may therefore be reasonably suggested that KTP, FLM, and MLX could all be administered to effect slight changes in acute phase proteins.
18
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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
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2018
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tom 69
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nr 6
19

Prostaglandins and inflammation: the cyclooxygenase controversy

72%
Morteau O.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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tom 48
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nr 6 Spec.Iss.
473-480
20

Evaluation of serum and urine neutrophil gelatinase-associated lipocalin and cystatin C as biomarkers of acute kidney injury in horses

72%
Siwinska N., Zak A., Paslawska U.
Journal of Veterinary Research
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2021
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tom 65
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nr 2
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