Galangin Mitigates Oxidative Damage Induced by Environmental Stresses in Skin Keratinocytes

Particulate matter 2.5 (PM_2.5) is a major air contaminant that causes skin damage by interacting with ultraviolet (UV) radiation. Exposure to those environmental stresses leads to oxidative skin damage and apoptosis. Although galangin is a natural flavonoid with antioxidant and several bioactive properties, its antioxidative effects following combined PM_2.5 and UVB exposure have not been fully investigated. Therefore, the aim of this study was to investigate the protective effect of galangin against PM_2.5- and UVB-induced oxidative stress and apoptosis in keratinocytes. Human HaCaT keratinocytes were pre-treated with galangin and treated with PM_2.5 and/or UVB. Intracellular reactive oxygen species (ROS) levels, lipid peroxidation, protein oxidation, DNA damage, mitochondrial damage, apoptotic protein expression, and cellular apoptosis were assessed using flow cytometry, confocal microscopy, and western blotting. Galangin reduced ROS levels, lipid peroxidation, protein oxidation, DNA damage, mitochondrial damage, and cellular apoptosis caused by PM_2.5 and/or UVB exposure. Additionally, galangin attenuated PM_2.5- and UVB-induced upregulation of apoptosis-related proteins and restored the expression of anti-apoptotic proteins. PM_2.5 and/or UVB enhanced cellular apoptosis by activating the mitogen-activated protein kinase (MAPK) signaling pathway. Notably, combined treatment with MAPK inhibitors and galangin demonstrated a protective effect against PM_2.5- and/or UVB-induced apoptosis. Galangin protected human keratinocytes against PM_2.5- and/or UVB-induced cellular damage by inhibiting MAPK signaling, suggesting that it may be a beneficial ingredient in skin care products designed to safeguard the skin from the detrimental effects of environmental stress.