过敏性和炎症性皮肤病中的氧化应激。

Yoshimichi Okayama
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引用次数: 250

摘要

皮肤暴露于内源性和环境促氧化剂中,导致有害的活性氧(ROS)的产生。由此产生的氧化应激会损害蛋白质、脂质和DNA。活性氧和抗氧化剂之间的不平衡会导致氧化应激水平升高。一些证据表明,过敏性和炎症性皮肤病,如特应性皮炎、荨麻疹和牛皮癣是由氧化应激介导的。例如,来自特应性皮炎患者的单核细胞对zymosan(一种toll样受体2 (TLR2)配体)产生ROS,提示金黄色葡萄球菌可能通过产生ROS损害病变皮肤。肥大细胞主要在FceRI聚集后产生胞内ROS;这些ROS可能在诱导几种生物反应中作为次级信使。本文综述了活性氧在过敏性和炎症性皮肤病发病机制中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oxidative stress in allergic and inflammatory skin diseases.

The skin is exposed to endogenous and environmental pro-oxidant agents, leading to the harmful generation of reactive oxygen species (ROS). The resulting oxidative stress damages proteins, lipids, and DNA. An imbalance between ROS and antioxidants can lead to an elevated oxidative stress level. Some evidence indicates that allergic and inflammatory skin diseases like atopic dermatitis, urticaria and psoriasis are mediated by oxidative stress. For example, monocytes from patients with atopic dermatitis are primed to generate ROS in response to zymosan, a Toll-like receptor 2 (TLR2) ligand, suggesting that Staphylococcus aureus may damage lesional skin of the disease by production of ROS. Mast cells generate mainly intracellular ROS following the aggregation of FceRI; these ROS may act as secondary messengers in the induction of several biological responses. The present review summarizes the involvement of ROS in the pathogenesis of allergic and inflammatory skin diseases.

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