Apigenin prevents oxidative stress and mitochondrial damage caused by particulate matter 2.5 in skin cells

Apigenin, a natural flavonoid, exhibits diverse pharmacological effects including antioxidant property. The present study evaluated the protective effects of apigenin on human HaCaT keratinocytes against damage induced by particulate matter 2.5 (PM2.5). Apigenin suppressed PM2.5-induced production of reactive oxygen species (ROS). Apigenin mitigated excessive accumulation of mitochondrial Ca2+ caused by PM2.5, along with a reduction in ATP, production of mitochondrial ROS, and depolarization of the mitochondrial membrane potential, thereby inhibiting cytochrome c release from mitochondria to the cytosol. Apigenin decreased the cellular apoptosis and the levels of proapoptotic phosphorylated p53, B-cell lymphoma-2-associated X protein, cleaved caspase-9, and cleaved caspase-3, which were all elevated by PM2.5. Furthermore, apigenin reversed the negative effects of PM2.5 on cell proliferation and the levels of proteins involved in advancing the G0/G1 phase of cell cycle. These findings indicate that apigenin can potentially mitigate skin cell damage induced by PM2.5.