INT8413
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
These data are compatible with the hypothesis that the sensory abnormalities observed in patients with RP may depend on estradiol-induced changes in SPGN, resulting in a sympathetically-dependent production of cyclooxygenase products of arachidonic acid. | |||||||||||||||
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Systemic acetylsalicylic acid and mefenamic acid, in doses known to produce cyclooxygenase inhibition, produced limited or no analgesia using a duodenal distension model and a behavioral scale for assessment. | |||||||||||||||
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Western blotting demonstrated general expression of cyclooxygenase-1 in test tissues and cyclooxygenase-2 within the brain and cerebellum. | |||||||||||||||
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This is consistent with the apparent impossibility for the expression of cyclooxygenase active protein from cyclooxygenase-3 mRNA in the rat. | |||||||||||||||
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Western blotting demonstrated general expression of cyclooxygenase-1 in test tissues and cyclooxygenase-2 within the brain and cerebellum. | |||||||||||||||
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Reverse transcription-polymerase chain reaction analysis of aorta, brain, cerebellum, heart, and lung showed general expression of cyclooxygenase-1 and cyclooxygenase-3 mRNA and particular expression of cyclooxygenase-2 mRNA in brain and cerebellum. | |||||||||||||||
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Reverse transcription-polymerase chain reaction analysis of aorta, brain, cerebellum, heart, and lung showed general expression of cyclooxygenase-1 and cyclooxygenase-3 mRNA and particular expression of cyclooxygenase-2 mRNA in brain and cerebellum. | |||||||||||||||
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The results of the present studies also reveal that melatonin may influence the expression of Cu-Zn SOD, catalase, cyclooxygenase as well as alpha-actinin whose levels were found to be altered, following piroxicam treatment. | |||||||||||||||
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By Northern analysis, only PGHS-2 is expressed by the immortalized rat osteoblastic cell line, Py1a, while only PGHS-1 is expressed by the rat osteosarcoma cell line, ROS 17/2.8. | |||||||||||||||
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A 5-week study was carried out in rats using a leukotriene biosynthesis inhibitor (MK-886; 3-[1-(4-chlorobenzyl)-3-t-butylthio-5-isopropylindol-2-yl]-2,2- dimethylpropanoic acid) at a dose of 300 mg.kg-1 x day-1, this being sufficient to produce > 90% inhibition of ex vivo leukotriene B4 synthesis in rat blood, and a cyclooxygenase inhibitor (indomethacin, 4 and 6 mg.kg-1 x day-1) to ascertain whether inhibition of leukotriene biosynthesis would potentiate or inhibit the toxicity associated with the administration of nonsteroidal anti-inflammatory drugs (NSAIDs), in particular the gastrointestinal damage. | |||||||||||||||
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IMPLICATIONS: Spinal injection of the alpha2-adrenergic agonist clonidine and the cyclooxygenase inhibitor ketorolac results in a synergistic interaction for antinociception in normal animals, suggesting that the combination of these drugs will enhance rather than detract from the analgesia of either alone. | |||||||||||||||
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Although both alpha2-adrenergic agonists and cyclooxygenase inhibitors produce analgesia, their exact sites of action and interaction remain unclear. | |||||||||||||||
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The potency difference is similar to that for inhibition of cyclooxygenase in brain tissue and supports the hypothesis that cyclooxygenase products are involved in prolonged spinal nociceptive transmission. | |||||||||||||||
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Furthermore, the effect of a high dose of 25 mg/kg of the S(+) enantiomer on release of cyclooxygenase products from the various tissues was much longer lasting than that of an identical dose of the R(-) enantiomer. | |||||||||||||||
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With the S(+) enantiomer and the racemate dose-dependent inhibition of release of cyclooxygenase products of arachidonate metabolism in all tissues tested was observed, while release of leukotriene (LT) C4 was inhibited in gastric mucosa, but not in jejunum and lung. | |||||||||||||||
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In the present study, we examined the changes of cyclooxygenase-1 and cyclooxygenase-2 protein expression in several regions of the CNS associated with pain perception, and the role of spinal cyclooxygenase activity in the development of allodynia following nerve injury. | |||||||||||||||
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In contrast, cyclooxygenase-1 protein was not detectable in any of the neural tissues examined one, three, and 14 days after nerve injury. | |||||||||||||||
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Effects of cyclooxygenase products of arachidonic acid metabolism on cutaneous nociceptive threshold in the rat. | |||||||||||||||
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The edema was accompanied by an increase in 5-lipoxygenase products, and the hyperalgesia coincided with the formation of both cyclooxygenase and 5-lipoxygenase products. | |||||||||||||||
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MATERIALS AND METHODS: Cerebral infarcted rats underwent cumulative intravenous administration of the selective cyclooxygenase-1 inhibitor SC-560 (Sigma), the selective cyclooxygenase-2 inhibitor rofecoxib (Kemprotec, Middlesbrough, United Kingdom) or the nonselective cyclooxygenase inhibitor FYO-750 hourly plus a single intravenous administration of SC-560, rofecoxib or SC-560 plus rofecoxib. | |||||||||||||||
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General Comments
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