“…UV exposure enhances ROS/RNS production [4,5,6], and the free radicals cause skin damage including apoptosis by interacting with DNAs, RNAs, and proteins [7]. Several lines of evidence have pointed to the implication of mitogen-activated protein kinase, aryl hydrocarbon receptor, transcription factors, such as nuclear factor-κB and nuclear factor erythroid 2-related factor 2, or matrix metalloproteinase in the degradation of dermal connective tissue following oxidative stress-induced skin damage [8,9,10,11,12,13,14,15]. …”