1988
DOI: 10.1111/j.2042-7158.1988.tb05178.x
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Effects of indomethacin and diclofenac on some functions of polymorphonuclear neutrophils

Abstract: The effects in-vitro of two non-steroidal anti-inflammatory drugs, diclofenac and indomethacin, have been studied on human polymorphonuclear functions. Adhesivity and chemotaxis were decreased by the two drugs, but in a manner that varied with the attractant used. As shown by the nitro blue tetrazolium slide test, all cells remained active but the production of oxygen metabolites by opsonized zymosan was decreased in the presence of diclofenac.

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Cited by 7 publications
(4 citation statements)
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“…Otherwise, it is well known that some NSAIDs inhibit PMN activity by reduction of the oxidative metabolism and therefore a rate of free radicals generated at the inflammatory site (Berradia et al, 1988;Yuda et al, 1991). It is well known that the inhibitory effect of some NSAIDs on PMN O 2…”
Section: But Enhances Omentioning
confidence: 99%
“…Otherwise, it is well known that some NSAIDs inhibit PMN activity by reduction of the oxidative metabolism and therefore a rate of free radicals generated at the inflammatory site (Berradia et al, 1988;Yuda et al, 1991). It is well known that the inhibitory effect of some NSAIDs on PMN O 2…”
Section: But Enhances Omentioning
confidence: 99%
“…We demonstrated in vivo that indomethacin inhibited the IL-8-induced infiltration of leukocytes. Indomethacin was also reported to inhibit adhesivity and chemotaxis of neutrophils in response to zymosan-activated serum or N-formyl-methionyl-leucyl-phenylalanine (FMLP) [26] and the release of lysosomal enzymes and the production of superoxide anions by neutrophils [27].…”
Section: Discussionmentioning
confidence: 99%
“…of local oropharyngeal inflammation and pain are mouthwashes, sprays and gargles, whose advantages over other formulations include fewer side effects and drug interactions, and particularly their greater contact and activity at the oropharyngeal site where the main inflammatory mediators are released. The main mechanism of action explaining the activity of NSAIDs is the inhibition of prostaglandin synthesis, however it has been reported that some NSAIDs can also scavenge free radicals [12][13][14][15][16] and inhibit the respiratory bursts of human neutrophils and the related release of ROS/RNS [17][18][19][20], which indicates the presence of an important additional mechanism that needs to be taken into account and investigated when making a pharmacological evaluation. Diclofenac-choline (DC), (obtained by a new salification process of diclofenac) has recently been proposed in the spray formulation for the symptomatic treatment of oropharyngeal inflammatory conditions and pain.…”
Section: Introduction ▼mentioning
confidence: 99%
“…With reference to local oropharyngeal inflammation and pain, topical formulation of NSAIDs such as flurbiprofen gel, ketorolac rinse or diclofenac itself have been found to lead to useful clinical results. Activated PMNs are present during oropharyngeal inflammation and various authors have challenged NSAIDs and diclofenac with neutrophil respiratory bursts releasing ROS/RNS, and gen-erally concluded that NSAIDs and diclofenac have an inhibitory effect [17][18][19][20]. However, these data have been obtained using relatively small concentrations and long incubation times of 30 or 60 min neither of which apply to the frequent short time associated with the practical use of NSAID-containing mouthwashes or sprays.…”
mentioning
confidence: 99%