Protective effects of astaxanthin on particulate matter 2.5‑induced senescence in HaCaT keratinocytes via maintenance of redox homeostasis

Abstract

Particulate matter 2.5 (PM_2.5) imposes a heavy burden on the skin and respiratory system of human beings, causing side effects such as aging, inflammation and cancer. Astaxanthin (ATX) is a well-known antioxidant widely used for its anti-inflammatory and anti-aging properties. However, few studies have investigated the protective effects of ATX against PM_2.5-induced senescence in HaCaT cells. In the present study, the levels of reactive oxygen species (ROS) and antioxidant enzymes were measured after treatment with PM_2.5. The results revealed that PM_2.5 generated excessive ROS and reduced the translocation of nuclear factor erythroid 2-related factor 2 (NRF2), subsequently reducing the expression of antioxidant enzymes. However, pretreatment with ATX reversed the ROS levels as well as the expression of antioxidant enzymes. In addition, ATX protected cells from PM_2.5-induced DNA damage and rescued PM_2.5-induced cell cycle arrest. The levels of senescence-associated phenotype markers, such as interleukin-1β, matrix metalloproteinases, and β-galactosidase, were increased by exposure to PM_2.5, however these effects were reversed by ATX. After interfering with NRF2 mRNA expression and exposing cells to PM_2.5, the levels of ROS and β-galactosidase were higher compared with siControl RNA cells exposed to PM_2.5. However, ATX inhibited ROS and β-galactosidase levels in both the siControl RNA and the siNRF2 RNA groups. Thus, ATX protects HaCaT keratinocytes from PM_2.5-induced senescence by partially inhibiting excessive ROS generation via the NRF2 signaling pathway.