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炎症刺激会加重紫外线A照射对J774细胞的影响。

Inflammatory stimulus worsens the effects of UV-A exposure on J774 cells.

作者信息

Chiarelli-Neto Orlando, Garcez Michelle Lima, Pavani Christiane, Martins Waleska, de Abreu Quintela Castro Fernanda Cristina, Ambrosio Roberta Passamani, Meotti Flavia Carla, Baptista Mauricio S

机构信息

Departamento de Bioquimica, Instituto de Química IQUSP, Universidade de São Paulo, Brazil; Centro Universitário do Espírito Santo-UNESC, Brazil.

Centro Universitário do Espírito Santo-UNESC, Brazil.

出版信息

J Photochem Photobiol B. 2023 Feb;239:112647. doi: 10.1016/j.jphotobiol.2023.112647. Epub 2023 Jan 4.

DOI:10.1016/j.jphotobiol.2023.112647
PMID:36634432
Abstract

UV-A radiation affects skin homeostasis by promoting oxidative distress. Endogenous photosensitizers in the dermis and epidermis of human skin absorb UV-A radiation forming excited states (singlet and triplet) and reactive oxygen species (ROS) producing oxidized compounds that trigger biological responses. The activation of NF-kB induces the expression of pro-inflammatory cytokines and can intensify the generation of ROS. However, there is no studies evaluating the cross talks between inflammatory stimulus and UV-A exposure on the levels of redox misbalance and inflammation. In here, we evaluated the effects of UV-A exposure on J774 macrophage cells previously challenged with LPS in terms of oxidative distress, release of pro-inflammatory cytokines, and activation of regulated cell death pathways. Our results showed that LPS potentiates the dose-dependent UV-A-induced oxidative distress and cytokine release, in addition to amplifying the regulated (autophagy and apoptosis) and non-regulated (necrosis) mechanisms of cell death, indicating that a previous inflammatory stimulus potentiates UV-A-induced cell damage. We discuss these results in terms of the current-available skin care strategies.

摘要

紫外线A辐射通过促进氧化应激影响皮肤稳态。人体皮肤真皮和表皮中的内源性光敏剂吸收紫外线A辐射,形成激发态(单线态和三线态)和活性氧(ROS),产生引发生物反应的氧化化合物。NF-κB的激活诱导促炎细胞因子的表达,并可加剧ROS的产生。然而,尚无研究评估炎症刺激与紫外线A暴露在氧化还原失衡和炎症水平上的相互作用。在此,我们评估了紫外线A暴露对先前用脂多糖(LPS)刺激的J774巨噬细胞在氧化应激、促炎细胞因子释放以及调节性细胞死亡途径激活方面的影响。我们的结果表明,LPS增强了紫外线A诱导的剂量依赖性氧化应激和细胞因子释放,此外还放大了细胞死亡的调节机制(自噬和凋亡)和非调节机制(坏死),表明先前的炎症刺激增强了紫外线A诱导的细胞损伤。我们根据当前可用的皮肤护理策略讨论了这些结果。

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