Inflammatory stimulus worsens the effects of UV-A exposure on J774 cells.
J Photochem Photobiol B
; 239: 112647, 2023 Feb.
Article
en En
| MEDLINE
| ID: mdl-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.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Lipopolisacáridos
/
Estrés Oxidativo
Límite:
Humans
Idioma:
En
Año:
2023
Tipo del documento:
Article