NAD(+) administration profoundly decreases UVC-induced skin damage by attenuating oxidative stress, inflammation, DNA damage and apoptosis

Ultraviolet (UV) radiation is a major cause of multiple major skin diseases including skin cancer. It is crucial to discover new agents that can produce profound protective effects on UV-produced skin damage. Using a mouse model, in this study we determined the effects of NAD(+) on UVC-induced skin damage and investigated the mechanisms underlying the effects, obtaining the following discoveries: First, UVC-induced skin’s green autofluorescence (AF) was highly correlated with the extent of UVC-indued skin’s damage; second, NAD(+) administration profoundly decreased UVC-induced skin damage; third, NAD(+) administration significantly attenuated UVC-induced decreases in the levels of mitochondrial superoxide dismutase and catalase; fourth, NAD(+) administration significantly attenuated UVC-induced increase in the level of cyclooxygenase (COX) 2 - a marker of inflammation; fifth, NAD(+) administration profoundly attenuated UVC-induced increase in double-strand DNA (dsDNA) damage; and sixth, NAD(+) administration profoundly attenuated UVC-induced decreases in the ratios of Bcl-2/Bax - an index of apoptosis. Collectively, our study has found that NAD(+) administration can profoundly decrease UVC-induced skin damage by attenuating oxidative stress, inflammation, DNA damage, and apoptosis, suggesting great potential of NAD(+) as a protective agent for UVC-induced skin damage. Moreover, our study has further indicated that the skin’s green AF is a biomarker for predicting UVC-induced skin damage.