Fucoxanthin ameliorates PM2.5-mediated skin cell inflammation and senescence.

Fucoxanthin is a naturally derived carotenoid in marine brown algae that has potential curative benefits for treating diseases such as cancer, diabetes, and obesity. Exposure to particulate matter with a diameter of ≤2.5 µm (PM_2.5) is associated with the occurrence of cardiac disorders, cancer, and senescence. The primary objective of this study was to determine the protective effects of fucoxanthin against PM_2.5-induced dysfunction of human HaCaT keratinocytes. Fucoxanthin decreased PM_2.5-induced production of reactive oxygen species and mitigated lipid peroxidation, DNA damage, and depolarization of the mitochondrial membrane potential. Fucoxanthin inhibited PM_2.5-mediated activation of nuclear factor κB and Nod-like receptor family protein 3 inflammasome and the release of proinflammatory cytokines such as interleukin (IL)-1, IL-6, and cyclooxygenase-2. Additionally, fucoxanthin decreased dysfunctional cell proliferation and reversed the cell cycle arrest in the G₀/G₁ phase. Docking and network analyses revealed that fucoxanthin interacted with seven major proteins related to inflammation and senescence. Senescence-associated β-galactosidase and matrix metalloproteinases were downregulated by fucoxanthin following exposure to PM_2.5. Conclusively, fucoxanthin attenuates the cellular oxidative stress caused by PM_2.5 and suppresses inflammatory responses and senescence, thereby implying its potential in alleviating PM_2.5-induced skin damage.