Topical application of a selective cyclooxygenase inhibitor suppresses UVB mediated cutaneous inflammation
Topical application of a selective cyclooxygenase inhibitor suppresses UVB mediated cutaneous inflammation
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DOI：
10.1016/s0090-6980(00)00089-7
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发表时间：
2000-10-01
影响因子：
2.9
通讯作者：
Oberyszyn, TM
中科院分区：
文献类型：
--
作者：
Wilgus, TA;Ross, MS;Oberyszyn, TM
中波紫外线(UVB)辐射是皮肤损伤的主要原因，也是人类皮肤癌最重要的致病因素。UVB照射可引起炎症反应，表现为水肿、真皮白细胞渗入、晒伤细胞形成、环氧合酶-2(COX-2)基因表达以及随后前列腺素的产生和释放增加。这种由UVB辐射引起的炎症过程与肿瘤的形成有关。最近，一种特异性的COX-2抑制剂塞来昔布被开发出来，它可以在不抑制环氧合酶-L(COX-1)细胞保护功能的情况下抑制COX-2诱导的炎症反应。本研究比较了局部应用塞来昔布(一种特异性的COX-2抑制剂)和布洛芬(一种非特异性的COX抑制剂)对UVB诱导的急性皮肤炎反应的影响。我们发现，COX-2的特异性抑制有效地减少了UVB介导的炎症的许多参数，包括水肿、真皮中性粒细胞的浸润和激活、前列腺素E-2(PGE(2))水平和晒伤细胞的形成。通过抑制这种炎症反应，塞来昔布局部治疗可能最终有效地防止UVB诱导的皮肤肿瘤发展。(C)2000 Elsevier Science Inc.保留所有权利。
Ultraviolet B (UVB) radiation causes much of the cutaneous damage after both acute and long-term exposure, and is also the most important etiologic agent in human skin cancer. UVB exposure initially induces an inflammatory response characterized by edema, dermal infiltration of leukocytes, sunburn cell formation, as well as the induction of cyclooxygenase-2 (COX-2) gene expression and subsequent increase in the production and release of prostaglandins. This process of inflammation induced by UVB exposure has been linked to tumor formation. Recently, a specific COX-2 inhibitor, Celecoxib, was developed, which inhibits COX-2-induced inflammation without inhibiting the cytoprotective function of cyclooxygenase-l (COX-1). The present study compared the effects of topical treatment with Celecoxib (a specific COX-2 inhibitor) and Ibuprofen (a nonspecific COX inhibitor) on the acute UVB-induced cutaneous inflammatory response. We show that the specific inhibition of COX-2 effectively reduced many parameters of UVB-mediated inflammation, including edema, dermal neutrophil infiltration and activation, prostaglandin E-2 (PGE(2)) levels and the formation of sunburn cells. By inhibiting this inflammatory response, topical Celecoxib treatment may ultimately be effective in preventing UVB-induced tumor development in the skin. (C) 2000 Elsevier Science Inc. All rights reserved.