scholarly journals Nonsteroidal Anti-Inflammatory Drugs Alter the Human Mesothelial Pleural Permeability via Ion Cellular Transportation by Inhibiting Prostaglandin Synthesis

Respiration ◽  
2012 ◽  
Vol 84 (1) ◽  
pp. 62-68 ◽  
Author(s):  
Vasileios K. Kouritas ◽  
Charalambos Zisis ◽  
Ion Bellenis ◽  
Konstantinos I. Gourgoulianis ◽  
Paschalis A. Molyvdas ◽  
...  
Keyword(s):  
Prostaglandin Synthesis ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Migrating action potential complex of cholera: a possible prostaglandin-induced response.

1977 ◽  
Vol 232 (5) ◽  
pp. E529 ◽  
Author(s):  
J R Mathias ◽  
G M Carlson ◽  
G Bertiger ◽  
J L Martin ◽  
S Cohen
Keyword(s):  
Action Potential ◽  
Propagation Velocity ◽  
Secretory Component ◽  
Prostaglandin Synthesis ◽  
Induced Response ◽  
Prostaglandin F2alpha ◽  
New Zealand White Rabbits ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Potential Complex

Distal ileal loops of New Zealand white rabbits exposed to cholera toxin demonstrated the presence of a highly organized myoelectric pattern defined as the migrating action potential complex (MAPC). We investigated the mechanism by which cholera enterotoxin stimulates MAPC activity. Certain anti-inflammatory drugs have altered the secretory component of cholera diarrhea. We investigated effects of these anti-inflammatory drugs on the MAPC. Indomethacin, 5.0 mg/kg iv, abolished all MAPC activity. Indomethacin, 1.5 mg/kg iv, or acetylsalicylic acid, 150 mg/kg given intragastrically, altered propagation velocity and at times its direction of propagation, but did not abolish the MAPC. An infusion of prostaglandin F2alpha, 2 microng/kg per min intraluminally, induced MAPC activity similar to that of the cholera complex. Indomethacin, 5.0 mg/kg iv, produced no significant changes in number of complexes or propagation velocity. These observations suggested that inhibition of the cholera complex by indomethacin may result from the alteration of prostaglandin synthesis and that prostaglandins may initiate the motility component of cholera diarrhea.

Naproxen (naprosyn) and ketoprofen (orudis)

1974 ◽  
Vol 12 (7) ◽  
pp. 25-27
Keyword(s):  
Prostaglandin Synthesis ◽  
New Drugs ◽  
Inflammatory Activity ◽  
Inhibit Prostaglandin Synthesis ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Low Incidence ◽  
Gastric Irritation

Naproxen (Naprosyn - Syntex) and ketoprofen (Orudis - M & B) are new drugs for treating various forms of arthropathy. For both drugs the manufacturers claim good anti-inflammatory activity with a low incidence of unwanted effects, particularly gastric irritation, in comparison with other non-steroidal anti-inflammatory drugs. If these claims can be substantiated these preparations would be valuable. Like aspirin and other non-steroidal anti-inflammatory drugs they both inhibit prostaglandin synthesis. Both are chemically related to other such drugs, for example ibuprofen (Brufen - Boots).

scholarly journals Pathogenesis of Nonsteroidal Anti-Inflammatory Drug Gastropathy: Clues to Preventative Therapy

1999 ◽  
Vol 13 (2) ◽  
pp. 123-127 ◽  
Author(s):  
Salim MA Bastaki ◽  
John L Wallace
Keyword(s):  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Barrier Properties ◽  
Prostaglandin Synthesis ◽  
Preventative Therapy ◽  
Mucosal Integrity ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Reduced Toxicity ◽  
Chronic Use

Gastric ulceration and bleeding are major impediments to the chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs). The development of effective therapies for prevention of these adverse effects requires better understanding of their pathogenesis. Several features of NSAIDs contribute to the development of damage in the stomach, including the topical irritant effects of these drugs on the epithelium, impairment of the barrier properties of the mucosa, suppression of gastric prostaglandin synthesis, reduction of gastric mucosal blood flow and interference with the repair of superficial injury. The presence of acid in the lumen of the stomach also contributes to the pathogenesis of NSAID-induced ulcers and bleeding in a number of ways. Acid impairs the restitution process, interferes with hemostasis and can inactivate several growth factors that are important in mucosal integrity and repair. Profound suppression of gastric acid secretion has been shown to be effective in preventing NSAID-induced ulceration. There is a strong possibility that new NSAIDs entering the market will have greatly reduced toxicity in the gastrointestinal tract.

scholarly journals Cytokine control in human endometrium

Reproduction ◽  
2001 ◽  
pp. 3-19 ◽  
Author(s):  
RW Kelly ◽  
AE King ◽  
HO Critchley
Keyword(s):  
Direct Action ◽  
Progesterone Receptors ◽  
Interleukin 10 ◽  
Prostaglandin Synthesis ◽  
Leukaemia Inhibitory Factor ◽  
Interleukin 12 ◽  
Prostaglandin E ◽  
Inflammatory Drugs ◽  
Cytokine Synthesis ◽  
Anti Inflammatory

Cytokines within endometrium participate in both menstruation and implantation but also contribute to the defence mechanisms of the mucosal epithelium. Endometrium is under the control of steroid hormones, particularly progesterone and, thus, control of cytokines by this steroid is important. Although appreciable numbers of progesterone receptors are not found in endometrial leucocytes, progesterone can modulate cytokines by acting on uterine cells expressing the receptor. The NFkappaB pathway is important in the control of cytokine synthesis and can modulate production of chemokines, matrix metalloproteinases and the inducible prostaglandin synthesis enzyme COX-2. NFkappaB activity can be inhibited by progesterone by either stimulating synthesis of IkappaB, the molecule that restrains NFkappaB in the cytosol, or after binding to the nuclear receptor, competing with NFkappaB for recognition sites on the relevant gene. In this way, progesterone can limit pro-inflammatory pathways. The major palliatives for endometrial dysfunctions such as menorrhagia and dysmenorrhoea have been the non-steroidal anti-inflammatory drugs that inhibit prostaglandin synthesis. Prostaglandins have major effects on cytokine production but the direct action of prostaglandin E on leucocytes is not a pro-inflammatory response but is to stimulate interleukin 10 and inhibit interleukin 12 synthesis. The likely effect of the non-steroidal anti-inflammatory drugs is on the cells surrounding the small blood vessels, where a synergistic action between prostaglandin and chemokine will induce leucocyte entry and activation leading to lysis of connective tissue and menstruation. At the time of implantation, tight control of cytokine synthesis is required. Although leukaemia inhibitory factor is essential to implantation, the mouse knockout models show that the prostaglandin system is also essential but that there are mutually supportive pathways that compensate for the knockout of many cytokines.

scholarly journals Role of Cyclooxygenase Pathway and Risk Associated with Non-Steroidal Anti-inflammatory Drugs Therapy in Cardiovascular Diseases

2018 ◽  
Vol 3 (3) ◽  
pp. 270
Author(s):  
Vinay Kumar ◽  
Lilly Ganju ◽  
Iti Garg
Keyword(s):  
Vascular Wall ◽  
Prostaglandin Synthesis ◽  
Cyclooxygenase 2 ◽  
Cardiovascular Risks ◽  
Membrane Phospholipids ◽  
Cyclooxygenase 1 ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Prostacyclin Production

<p>Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the cyclooxygenase enzyme activity through different<br />mechanisms and prevent inflammation. But they all have different risks associated with them. Some are associated with<br />gastrointestinal bleeding and some are strongly allied with the cardiovascular risks. Cyclooxygenase enzyme regulates<br />prostaglandin synthesis by converting arachidonic acid present at the sn-2 position of membrane phospholipids to<br />prostaglandin H2. Prostaglandin H2 is the precursor of all prostaglandins. There are two isoforms of cyclooxygenase<br />enzyme, cyclooxygenase-1 and cyclooxygenase-2 which differ in their active site due to an isoleucine to valine<br />substitution at amino acid 523 in cyclooxygenase-2. Cyclooxygenase-1 is constitutively expressed in platelets<br />where it helps in the formation of thromboxane whereas cyclooxygenase-2 is inductive form and is expressed in<br />the endothelial cells due to shear stress and forms prostacyclins. Both thromboxanes and prostacyclins maintain<br />the homeostasis of the vascular wall. During vascular injury prostacyclin production decreases as a result of which<br />thromboxane synthesis increases in the platelets which leads to platelet aggregation. Although, being strongly<br />associated with cardiovascular risks, NSAIDs are still prescribed to the patients to prevent pain according to their<br />condition. So this review aims to summarise the mechanism of cyclooxygenase pathway, possible mechanism of<br />action of NSAIDs and the risks of cardiovascular events associated with the use of NSAIDs.</p>

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