皮肤光损伤与氧化应激研究进展

发布时间：2018-06-04 03:20

本文选题：紫外线 + 光损伤　；参考：《临床皮肤科杂志》2017年09期

【摘要】：长期或大量紫外线照射后皮肤发生氧化应激,不仅从分子水平上改变了蛋白质、脂质、DNA等的结构和功能,同时于转录水平上激活丝裂原活化蛋白激酶通路、核转录因子通路、信号转导和转录激活因子通路,抑制核转录因子E2相关因子(Nrf)2通路等信号转导途径,引起皮肤细胞凋亡、细胞外基质降解,最终出现红斑、脱屑、皱纹、甚至肿瘤等光损伤表现。近年来针对氧化应激在光损伤发生及发展过程中的作用机制,以及光损伤的防治亦有较多新进展,该文从氧化应激角度对近年光损伤的发病机制和研究进展进行了回顾和总结,同时对其治疗前景进行展望。
[Abstract]:Oxidative stress occurs in the skin after long-term or massive ultraviolet irradiation, which not only changes the structure and function of proteins, lipids and DNA at the molecular level, but also activates the mitogen-activated protein kinase pathway and nuclear transcription factor pathway at the transcriptional level. Signal transduction and transcriptional activator pathway, inhibition of signal transduction pathway such as nuclear transcription factor E2 related factor and Nrff2 pathway, induce apoptosis of skin cells, degradation of extracellular matrix, and finally, erythema, desquamation, wrinkles, etc. Even the tumor and other light damage manifestations. In recent years, the mechanism of oxidative stress in the process of light injury, and the prevention and treatment of light injury have been reviewed and summarized from the perspective of oxidative stress. At the same time, the prospect of treatment was prospected.
【作者单位】：西南医科大学附属医院皮肤科;
【基金】：国家自然科学基金(No.31470950)资助项目
【分类号】：R751

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