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通过抑制环氧化酶-2治疗光化性角化病:二氯芬酸钠 3%在透明质酸 2.5 中的作用机制。

Treatment of actinic keratosis through inhibition of cyclooxygenase-2: Potential mechanism of action of diclofenac sodium 3% in hyaluronic acid 2.5.

机构信息

Cancer Sciences Unit, University of Southampton, Southampton, United Kingdom.

Department of Dermatology, La Paz University Hospital, Madrid, Spain.

出版信息

Dermatol Ther. 2019 May;32(3):e12800. doi: 10.1111/dth.12800. Epub 2019 Apr 9.

DOI:10.1111/dth.12800
PMID:30523664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6767532/
Abstract

Cyclooxygenase-2 (COX-2) and its metabolic product prostaglandin E (PGE ) are induced in response to growth factors, inflammatory cytokines, tumor promoters, activated oncogenes, and, in the skin, ultraviolet (UV) radiation. Accumulating evidence suggests a role for the COX-2/PGE pathway in tumorigenesis in various tissue types including cutaneous squamous cell carcinoma. There is also strong evidence for a role in the development of actinic keratoses (AKs) - common dysplastic lesions of the skin associated with UV radiation overexposure - considered as part of a continuum with skin cancer. Non-steroidal anti-inflammatory drugs (NSAIDs) exert their anti-inflammatory, analgesic, and antipyretic effects by reversibly or irreversibly acetylating COX isoforms, inhibiting downstream prostaglandins, and may have a chemopreventive role in malignancies, including skin cancer. Topical treatment of AK lesions with the NSAID diclofenac sodium 3% in combination with hyaluronic acid 2.5% has been shown to be effective and well tolerated, although the mechanism of action remains to be elucidated.

摘要

环氧化酶-2(COX-2)及其代谢产物前列腺素 E(PGE)是对生长因子、炎性细胞因子、肿瘤促进剂、激活的致癌基因,以及在皮肤中紫外线(UV)辐射的反应而产生的。越来越多的证据表明,COX-2/PGE 途径在各种组织类型的肿瘤发生中发挥作用,包括皮肤鳞状细胞癌。在光化性角化病(AK)的发生中也有很强的作用,AK 是一种常见的皮肤发育不良病变,与 UV 过度暴露有关,被认为是皮肤癌的一部分。非甾体抗炎药(NSAIDs)通过可逆或不可逆地乙酰化 COX 同工酶、抑制下游前列腺素,发挥其抗炎、镇痛和解热作用,并且可能在包括皮肤癌在内的恶性肿瘤中具有化学预防作用。已经证明,将 NSAID 双氯芬酸钠 3%与透明质酸 2.5%联合用于 AK 病变的局部治疗是有效且耐受良好的,尽管其作用机制仍有待阐明。

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