1993
DOI: 10.1097/00005373-199309000-00002
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Effect of Ibuprofen on the Inflammatory Response to Surgical Wounds

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Cited by 60 publications
(40 citation statements)
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“…In line with our finding COX-2 inhibition was reported to relieve inflammatory response in sponge implants model of wound healing and promotes the closure of excisional lesions [42,79]. However, Other studies, showed that COX inhibition does not affect wound healing [80,81] and other studies showed that COX-2 inhibition reduces the wound closure delay the healing [82,83]. This discrepancy in the results could be due to the differences in models, in species and in the route of administration; Salcido et al and Dong et al [81,82] have used a pressure ulcer or a burn model of wound healing, the lack of effect of COX inhibition on inflammation in these models could be attributed to the excessive damage and epidermal loss associated with these models [84,85], unlike our incisional wound model.…”
Section: Discussionsupporting
confidence: 84%
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“…In line with our finding COX-2 inhibition was reported to relieve inflammatory response in sponge implants model of wound healing and promotes the closure of excisional lesions [42,79]. However, Other studies, showed that COX inhibition does not affect wound healing [80,81] and other studies showed that COX-2 inhibition reduces the wound closure delay the healing [82,83]. This discrepancy in the results could be due to the differences in models, in species and in the route of administration; Salcido et al and Dong et al [81,82] have used a pressure ulcer or a burn model of wound healing, the lack of effect of COX inhibition on inflammation in these models could be attributed to the excessive damage and epidermal loss associated with these models [84,85], unlike our incisional wound model.…”
Section: Discussionsupporting
confidence: 84%
“…Additionally, the response to COX inhibition varied in different species, while COX inhibitors did not affect wound healing in hairless SKH-1 mice, they delayed healing in C57BL/6J mouse [83] and this could be explained by differences in genetic background [86] between species and even intra-species. Furthermore, the route of administration of the drugs would another factor explaining the discrepancy in the results; oral administration of COX inhibitor were found not to improve healing [82,83], indeed topical application would be more effective in wound healing than systemic [87,88].…”
Section: Discussionmentioning
confidence: 98%
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“…Cytotoxic antineoplastic agents (e. g. hydroxyurea, tyrosine kinase inhibitors, angiogenesis inhibitors [ 108,109 ] Systemic corticosteroids [ 110 ] Systemic nonsteroidal antiinflammatory drugs (NSAIDs) (e. g. ibuprofen, acetylsalicylic acid [111][112][113] ) Anticoagulants [ 114 ] Bisphosphonates [ 115 ] Morphine [ 116 ] microenvironment -the interactions between the various cell types and proteases involved -it is not surprising that the outcomes of using these factors in the treatment of chronic wounds have not been fully satisfactory. Further research is definitely required to uncover strategies that will improve their clinical effectiveness.…”
Section: Challenges and Perspectives In The Treatment Of Chronic Wounmentioning
confidence: 99%
“…This has been demonstrated by exogenously adding the stable PGE 2 analog 16,16-dimethyl prostaglandin E 2 -methyl ester (Brzozowski et al, 1993), PGHS inhibitors (Brzozowski et al, 1993;Dong et al, 1993;Fang et al, 1983;LeDuc et al, 1993;Sun et al, 2000), or agents that increase plasma PGE 2 levels (Gonul et al, 1993). There is some evidence to suggest that PGE 2 may be more important in the early stages of wound healing, causing increased fibrosis and decreased accumulation of macrophages by 7 days after injury (Talwar et al, 1996).…”
mentioning
confidence: 99%