The inhibitory effect of chlorogenic acid on oxidative stress and apoptosis induced by PM 2.5 in HaCaT keratinocytes.

Exposure to fine particulate matter with an aerodynamic diameter of less than 2.5 μm (PM 2.5 ) can cause oxidative damage and apoptosis in the human skin. Chlorogenic acid (CGA) is a bioactive polyphenolic compound with antioxidant, antifungal, and antiviral properties. The objective of this study was to identify the ameliorating impact of CGA that might protect human HaCaT cells against PM 2.5 . CGA significantly scavenged the reactive oxygen species (ROS) generated by PM 2.5 , attenuated oxidative cellular/organelle damage, mitochondrial membrane depolarization, and suppressed cytochrome c release into the cytosol. The application of CGA led to a reduction in the expression levels of Bcl-2-associated X protein, caspase-9, and caspase-3, while simultaneously increasing the expression of B-cell lymphoma 2. In addition, CGA was able to reverse the decrease in cell viability caused by PM 2.5 via the inhibition of extracellular signal-regulated kinase (ERK). This effect was further confirmed by the use of the mitogen-activated protein kinase kinase inhibitor, which acted upstream of ERK. In conclusion, CGA protected keratinocytes from mitochondrial damage and apoptosis via ameliorating PM 2.5 -induced oxidative stress and ERK activation.