INT35975
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The aim of our study was to investigate the effect of various cyclooxygenase (COX) inhibitors (namely, indomethacin [a nonselective COX inhibitor], nimesulide [a partially selective COX inhibitor] and celecoxib [a highly selective COX inhibitor]) on postoperative ileus in rats. | |||||||||||||||
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Role of spinal cyclooxygenase (COX)-2 on thermal hyperalgesia evoked by carageenan injection in the rat. | |||||||||||||||
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The purpose of the present study was to investigate the role of central cyclooxygenase (COX) pathways in the modulation of mechanical allodynia following compression of the left trigeminal ganglion. | |||||||||||||||
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The classically recognized target for NSAID action are the two isoforms of the cyclooxygenase (COX) gene, which is responsible for prostaglandin production. | |||||||||||||||
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These COX inhibitors failed to affect the depressor responses to BK. | |||||||||||||||
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The present study was designed to examine the influence of selective COX-2 inhibitors, such as rofecoxib and celecoxib, on gastric mucosal integrity in rats with adjuvant-induced arthritis. | |||||||||||||||
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Differential effect of selective cyclooxygenase-2 (COX-2) inhibitor NS 398 and diclofenac on formalin-induced nociception in the rat. | |||||||||||||||
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These results suggest that a selective COX-2 inhibitor is effective in the effector phase by its influence on macrophages that are responsible for nerve degeneration. | |||||||||||||||
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The present study delineates the intracellular ionic milieu in the colonocytes that could generate strong apoptotic signals where DMH-induced carcinogenesis was studied in the initiation stage in rats and its regression with the COX inhibitors. | |||||||||||||||
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Although DFU inhibited PGE(2) by one-third, it did not affect COX expression. 3. | |||||||||||||||
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Indomethacin and SC-560 significantly inhibited prostaglandin (PG) E(2), without significantly affecting COX-1 and COX-2 expression. | |||||||||||||||
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The present study was undertaken to determine the effects of cyclooxygenase (COX) inhibitors on the development of neuropathic pain in rats following chronic constriction injury (CCI). | |||||||||||||||
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Effect of COX-1 and COX-2 inhibition on induction and maintenance of carrageenan-evoked thermal hyperalgesia in rats. | |||||||||||||||
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Effect of COX-1 and COX-2 inhibition on induction and maintenance of carrageenan-evoked thermal hyperalgesia in rats. | |||||||||||||||
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METHODS: To evaluate the relative contribution of COX-1 and COX-2 in nociceptive transmission in the spinal cord, we assessed the effects of the selective COX-1 inhibitor SC 560, the selective COX-2 inhibitor celecoxib, and the nonselective COX inhibitor ketorolac on formalin-evoked behavior and spinal c-Fos-like immunoreactivity (FLI). | |||||||||||||||
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METHODS: To evaluate the relative contribution of COX-1 and COX-2 in nociceptive transmission in the spinal cord, we assessed the effects of the selective COX-1 inhibitor SC 560, the selective COX-2 inhibitor celecoxib, and the nonselective COX inhibitor ketorolac on formalin-evoked behavior and spinal c-Fos-like immunoreactivity (FLI). | |||||||||||||||
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METHODS: To evaluate the relative contribution of COX-1 and COX-2 in nociceptive transmission in the spinal cord, we assessed the effects of the selective COX-1 inhibitor SC 560, the selective COX-2 inhibitor celecoxib, and the nonselective COX inhibitor ketorolac on formalin-evoked behavior and spinal c-Fos-like immunoreactivity (FLI). | |||||||||||||||
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METHODS: To evaluate the relative contribution of COX-1 and COX-2 in nociceptive transmission in the spinal cord, we assessed the effects of the selective COX-1 inhibitor SC 560, the selective COX-2 inhibitor celecoxib, and the nonselective COX inhibitor ketorolac on formalin-evoked behavior and spinal c-Fos-like immunoreactivity (FLI). | |||||||||||||||
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For example, despite muscle atrophy there was no change in the activity of citrate synthase or COX, or the abundance of COX subunit mRNAs in plantaris muscle in glucocorticoid-treated rats [4], [6]. | |||||||||||||||
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We previously reported the effect of a cyclooxygenase (COX)-2 inhibitor, nimesulide, on experimental allergic neuritis (EAN) in both the induction and effector phases, in contrast to the usual COX inhibitor, which was effective only when administered in the induction phase. | |||||||||||||||
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