Piceatannol protects ARPE-19 cells against vitamin A dimer-mediated photo-oxidative damage through activation of Nrf2/NQO1 signalling

Piceatannol, abundant in grapes and red wine, may prevent photo-oxidative damage to the eyes. During the aging process, dimers of dietary vitamin A accumulate in retinal pigment epithelium (RPE) cells and photo-oxidation of these dimers causes RPE death. This death is associated with age-related retinal degenerative disease and blindness. In this study, we investigated the underlying mechanism of photo-oxidation-induced apoptotic inhibition using piceatannol. To mimic Vitamin A dimer-mediated photo-oxidation, ARPE-19 cells with accumulated vitamin A dimers were used as a model to study apoptosis. Cells were either pretreated with piceatannol or untreated and exposed to blue light-induced endoplasmic reticulum stress (ER stress). Apoptosis was then measured and piceatannol was noted to inhibit apoptosis and ER stress. The mechanism by which this protective effect of piceatannol occurs is through the nuclear factor erythroid-derived 2-related factor 2 (Nrf2)/NAD(P)H quinine oxidoreductase 1(NQO1) pathway, which is likely due to activation of Akt signalling.