INT35486
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Therefore several mechanisms could account for indomethacin in regulating the bioavailability of PGE2. | |||||||||||||||
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Whether changes in levels of PGE2 are primary or secondary causes of CRN remains unclear. | |||||||||||||||
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In normotensive and hypertensive humans, prostaglandins, particularly PGE2 and PGI2, affect blood pressure through control of vascular resistance, salt excretion, cardiac output, and renin secretion. | |||||||||||||||
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Intriguingly, changes in cAMP levels in response to particular PGE2 doses inversely correlate with their proliferative potency (compare Figs. 1A and 3A): Thus, mitogenic PGE2 doses either down regulate or do not ostensibly affect cAMP levels whereas anti or non-proliferative PGE2 concentrations do in all cases elevate cAMP. | |||||||||||||||
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Similarly, there is only a limited body of partially conflictive experimental data on the regulation of apoptosis in colorectal cancer cells by PGE2 [13,22-24]. | |||||||||||||||
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More recently, a study comparing EP receptor expression in nasal biopsies from aspirin intolerant and tolerant patients showed an up-regulation of EP1 and EP2 in structural cells from aspirin intolerant subjects [15]. | |||||||||||||||
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The objective of this study was to determine the effects of COX-2 inhibitors on amounts of PGE2 and IL-6 made by IL-1beta-stimulated gingival fibroblasts. | |||||||||||||||
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Several enzymes and regulatory pathways control the level of PGE2 both in colonic cells and in the intercellular environment of colonic tissue, Figure 1. | |||||||||||||||
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Finally, neither sodium nitroprusside nor zaprinast (both of which elevate cGMP levels) affected GM-CSF or PGE2 release. | |||||||||||||||
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The observed changes in PGE2, TNF alpha and annexin A2 corroborate anti-inflammatory effects of the diclofenac treatment in the overweight subjects. | |||||||||||||||
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To confirm the lack of apoptosis regulation by PGE2, we monitored Annexin V-binding via FACS analysis (Fig. 2B). | |||||||||||||||
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While sialic acid levels were not different between groups, responses of PGE2 and CRP on diclofenac treatment differed significantly from responses on placebo treatment (PGE2: treatment × time interaction p = 0.017; hsCRP: treatment × time interaction p = 0.0273). | |||||||||||||||
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In addition to changes in PGE2, diclofenac intervention also altered levels of other plasma oxylipids, increasing 5,6-dihydroxy-eicosatrienoic acid (5,6-DHET) and 20-HETE (20-hydroxyeicosatetraenoic acid) and decreasing the linoleate derived 9,10-dihydroxyoctadecenoic acid (9,10-DHOME). | |||||||||||||||
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Firstly, effects of diclofenac on known inflammatory markers CRP, PGE2 and sialic acid were assessed. | |||||||||||||||
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In our previous study, we showed that KSHV modulates host factors COX-2/PGE2 for its own advantage to promote its latent (persistent) infection. | |||||||||||||||
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Inhibition of PLA2 can effectively control both PGE2 and LTB4, but will also downregulate all the downstream AA metabolites including vasoactive eicosanoids, which has important physiological functions. | |||||||||||||||
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mol/l celecoxib (Figure 3 panels a [part iii] and c), suggesting that the celecoxib-mediated inhibition was dependent on PGE2. | |||||||||||||||
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Measurement of PGE2, IL-10 and IL-18 content in culture medium | |||||||||||||||
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It therefore appears that, regardless of menopausal status, it is the circulating level of celecoxib that is important, with low levels having little influence on PGE2, and higher doses decreasing PGE2. | |||||||||||||||
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M), while it had no effect on PGE2 production.
3.3. | |||||||||||||||
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