颗粒物2.5（PM2.5）给人类的皮肤和呼吸系统带来沉重负担，造成衰老、炎症和癌症等副作用。虾青素 (ATX) 是一种众所周知的抗氧化剂，因其抗炎和抗衰老特性而被广泛使用。然而，很少有研究探讨 ATX 对 PM2.5 诱导的 HaCaT 细胞衰老的保护作用。在本研究中，测量了PM2.5处理后活性氧（ROS）和抗氧化酶的水平。结果显示，PM2.5产生过量的ROS，并减少核因子红细胞2相关因子2（NRF2）的易位，从而降低抗氧化酶的表达。然而，ATX 预处理逆转了 ROS 水平以及抗氧化酶的表达。此外，ATX 还可以保护细胞免受 PM2.5 诱导的 DNA 损伤，并挽救 PM2.5 诱导的细胞周期停滞。暴露于 PM2.5 会增加与衰老相关的表型标记物（例如白细胞介素 1β、基质金属蛋白酶和 β-半乳糖苷酶）的水平，但这些影响会被 ATX 逆转。干扰NRF2 mRNA表达并将细胞暴露于PM2.5后，与暴露于PM2.5的siControl RNA细胞相比，ROS和β-半乳糖苷酶的水平更高。然而，ATX 抑制 siControl RNA 和 siNRF2 RNA 组中的 ROS 和 β-半乳糖苷酶水平。因此，ATX 通过 NRF2 信号通路部分抑制过量 ROS 生成，从而保护 HaCaT 角质形成细胞免受 PM2.5 诱导的衰老。版权所有：© 2024 Zhun 等人。

Particulate matter 2.5 (PM2.5) 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 PM2.5-induced senescence in HaCaT cells. In the present study, the levels of reactive oxygen species (ROS) and antioxidant enzymes were measured after treatment with PM2.5. 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 PM2.5-induced DNA damage and rescued PM2.5-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 PM2.5, however these effects were reversed by ATX. After interfering with NRF2 mRNA expression and exposing cells to PM2.5, the levels of ROS and β-galactosidase were higher compared with siControl RNA cells exposed to PM2.5. However, ATX inhibited ROS and β-galactosidase levels in both the siControl RNA and the siNRF2 RNA groups. Thus, ATX protects HaCaT keratinocytes from PM2.5-induced senescence by partially inhibiting excessive ROS generation via the NRF2 signaling pathway.Copyright: © 2024 Zhen et al.