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 (PM2.5) 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 PM2.5-induced dysfunction of human HaCaT keratinocytes. Fucoxanthin decreased PM2.5-induced production of reactive oxygen species and mitigated lipid peroxidation, DNA damage, and depolarization of the mitochondrial membrane potential. Fucoxanthin inhibited PM2.5-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 PM2.5. Conclusively, fucoxanthin attenuates the cellular oxidative stress caused by PM2.5 and suppresses inflammatory responses and senescence, thereby implying its potential in alleviating PM2.5-induced skin damage.