INT34085
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
We have previously found that TLR4-deficient (TLR4-/-) mice demonstrate decreased expression of mucosal PGE 2 and are protected against colitis-associated neoplasia. | |||||||||||||||
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Our results demonstrated that paeonol inhibited LPS induced expression of NO, PGE(2) and IL-6. | |||||||||||||||
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Agents that block PGE synthesis, nonsteroidal anti-inflammatory agents (NSAID), are widely used by people with renal insufficiency. | |||||||||||||||
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Inhibition of Egr-1 expression reduced substantially LPS-mediated induction of COX-2 and mPGES-1 expression, resulting in a decrease in PGE(2) production. | |||||||||||||||
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NS-398 treatment of injured mice decreased PGE(2) production compared to T (3.9 +/- 0.3 vs 3.1 +/- 0.4 pg/microg protein), and significantly decreased IL-6, NO, and TNF-alpha production. | |||||||||||||||
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Our immunoblots revealed reduced expressions of COX-1 and COX-2 at peak ulceration, associated with reduced synthesis of serum and mucosal PGE. | |||||||||||||||
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In the peritonitis model in mice, meloxicam was approximately twice as active as piroxicam, and more than 10 times as active as diclofenac in the suppression of PGE biosynthesis. | |||||||||||||||
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Rauwolscine (1 X 10(-8) and 1 X 10(-7) M) attenuated angiotensin II-induced PGE production and at a higher concentration (1 X 10(-6) M) reduced angiotensin III-induced PGE production. | |||||||||||||||
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Rauwolscine (1 X 10(-8) and 1 X 10(-7) M) attenuated angiotensin II-induced PGE production and at a higher concentration (1 X 10(-6) M) reduced angiotensin III-induced PGE production. | |||||||||||||||
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The alpha-2 agonist, clonidine, both inhibited the nonadrenergic neural contraction and enhanced PGE synthesis. | |||||||||||||||
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Yohimbine (1 X 10(-5) and 1 X 10(-4) M) also significantly reduced angiotensin II-induced prostaglandin E (PGE) synthesis. | |||||||||||||||
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Following treatment with low concentrations of NS-398 (0.1 microM), PGE(2) production was reduced dramatically, indicating inhibition of COX-2 activity. | |||||||||||||||
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CONCLUSION: This decrease in PGE(2) production in synovial fibroblasts could help elucidate the mechanism by which physical therapy, and in particular continuous passive motion, may decrease inflammatory mediators of the temporomandibular joint.
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Considering the protective effect of exogenous PGE(2) on aspirin-induced bronchoconstriction and the interdependence of PGE(2) and cisteinyl leukotriene production, a reduced PGE(2) synthesis may render aspirin-sensitive patients more susceptible to the inhibitory effect of NSAIDs drugs and also lead to an increase in cysteinyl leukotriene release. | |||||||||||||||
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Recent studies have reported that patients with AIAR have decreased activity of COX-2 and lower production of PGE(2) in the upper airway and peripheral blood cells. | |||||||||||||||
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RESULTS: Naproxen suppressed biosynthesis of PGE-M, prostacyclin metabolites and thromboxane metabolites and thrombomodulin levels. | |||||||||||||||
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