Protective effects of astaxanthin on particulate matter 2.5‑induced senescence in HaCaT keratinocytes via maintenance of redox homeostasis
Ao Xuan Zhen, Kyoung Kang, Mei Jing Piao, Pincha Devage Madushan Fernando, Herath Mudiyanselage Lakmini Herath, Jin Won Hyun
Abstract
Particulate matter 2.5 (PM<sub>2.5</sub>) 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<sub>2.5</sub>‑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<sub>2.5</sub>. The results revealed that PM2.5 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<sub>2.5</sub>‑induced DNA damage and rescued PM<sub>2.5</sub>‑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<sub>2.5</sub>, however these effects were reversed by ATX. After interfering with NRF2 mRNA expression and exposing cells to PM<sub>2.5</sub>, the levels of ROS and β‑galactosidase were higher compared with siControl RNA cells exposed to PM<sub>2.5</sub>. 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<sub>2.5</sub>‑induced senescence by partially inhibiting excessive ROS generation via the NRF2 signaling pathway.