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Nitrooxyethylation Reverses the Healing-SuppressantEffect of Ibuprofen

机译:硝基氧乙基化逆转了愈合抑制剂布洛芬的作用

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摘要

Nonsteroidal antiinflammatory drugs like ibuprofen impede tissue repair by virtue of retarding inflammation. The present study was undertaken to explore if linking of nitrooxyethyl ester to ibuprofen reverses its healing-depressant propensity. Nitrooxyethyl ester of ibuprofen (NOE-Ibu) was synthesized in our laboratory through a well-established synthetic pathway. NOE-Ibu was screened for its influence on collagenation, wound contraction and epithelialization phases of healing, and scar size of healed wound in three wound models, namely, incision, dead space, and excision wounds. Besides, its influence on the oxidative stress (levels of GSH and TBARS) was also determined in 10-day-old granulation tissue. NOE-Ibu was further screened for its antiinflammatory activity in rat paw edema model. NOE-Ibu promoted collagenation (increase in breaking strength, granulation weight, and collagen content), wound contraction and epithelialization phases of healing. NOE-Ibu also showed a significant antioxidant effect in 10-day-old granulation tissue as compared to ibuprofen. Results vindicate that the esterification of ibuprofen withnitrooxyethyl group reverses the healing-suppressant effect ofibuprofen. The compound also showed equipotent antiinflammatoryactivity as ibuprofen.
机译:非甾体抗炎药如布洛芬可通过延缓炎症来阻止组织修复。进行本研究以探讨硝基氧乙基酯与布洛芬的连接是否会逆转其愈合抑制倾向。布洛芬的硝基氧乙酯(NOE-Ibu)是在我们的实验室中通过完善的合成途径合成的。在三种伤口模型(即切口,死腔和切除伤口)中筛选了NOE-Ibu对胶原蛋白的形成,伤口的收缩和愈合的上皮形成阶段以及愈合伤口的疤痕大小的影响。此外,还测定了其对10日龄肉芽组织中氧化应激(GSH和TBARS水平)的影响。在大鼠爪水肿模型中进一步筛选了NOE-Ibu的抗炎活性。 NOE-Ibu促进胶原蛋白的形成(断裂强度,肉芽重量和胶原蛋白含量的增加),伤口的收缩和上皮愈合阶段。与布洛芬相比,NOE-Ibu在10天大的肉芽组织中也显示出显着的抗氧化作用。结果证明,布洛芬与硝基氧乙基逆转了甲氧西林的愈合抑制作用布洛芬。该化合物还显示出等效的抗炎作用活性为布洛芬。

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