AI Article Synopsis

  • Intense UVB radiation leads to increased reactive oxygen species and inflammation, which can cause skin damage.
  • AT-RvD1, a lipid mediator derived from omega-3, shows potential anti-inflammatory effects and helps reduce oxidative stress.
  • In tests on hairless mice, AT-RvD1 treatment was effective in minimizing skin inflammation and oxidative damage caused by UVB exposure, likely by activating the Nrf2 pathway to enhance the skin's antioxidant defense.

Article Abstract

Intense exposure to UVB radiation incites excessive production of reactive oxygen species (ROS) and inflammation. The resolution of inflammation is an active process orchestrated by a family of lipid molecules that includes AT-RvD1, a specialized proresolving lipid mediator (SPM). AT-RvD1 is derived from omega-3, which presents anti-inflammatory activity and reduces oxidative stress markers. The present work aims to investigate the protective effect of AT-RvD1 on UVB-induced inflammation and oxidative stress in hairless mice. Animals were first treated with 30, 100, and 300 pg/animal AT-RvD1 (i.v.) and then exposed to UVB (4.14 J/cm). The results showed that 300 pg/animal of AT-RvD1 could restrict skin edema, neutrophil and mast cell infiltration, COX-2 mRNA expression, cytokine release, and MMP-9 activity and restore skin antioxidant capacity as per FRAP and ABTS assays and control O production, lipoperoxidation, epidermal thickening, and sunburn cells development. AT-RvD1 could reverse the UVB-induced downregulation of Nrf2 and its downstream targets GSH, catalase, and NOQ-1. Our results suggest that by upregulating the Nrf2 pathway, AT-RvD1 promotes the expression of ARE genes, restoring the skin's natural antioxidant defense against UVB exposition to avoid oxidative stress, inflammation, and tissue damage.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10005614PMC
http://dx.doi.org/10.3390/molecules28052417DOI Listing

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