Delphinidins from Maqui Berry (Aristotelia chilensis) ameliorate the subcellular organelle damage induced by blue light exposure in murine photoreceptor-derived cells

Abstract

Abstract Background Blue light exposure is known to induce reactive oxygen species (ROS) production and increased endoplasmic reticulum stress, leading to apoptosis of photoreceptors. Maqui berry (Aristotelia chilensis) is a fruit enriched in anthocyanins, known for beneficial biological activities such as antioxidation. In this study, we investigated the effects of Maqui berry extract (MBE) and its constituents on the subcellular damage induced by blue light irradiation in mouse retina-derived 661W cells. Methods We evaluated the effects of MBE and its main delphinidins, delphinidin 3-O-sambubioside-5-O-glucoside (D3S5G) and delphinidin 3,5-O-diglucoside (D3G5G), on blue light-induced damage on retinal cell line 661W cells. We investigated cell death, the production of ROS, and changes in organelle morphology using fluorescence microscopy. The signaling pathway linked to stress response was evaluated by immunoblotting in the whole cell lysates or nuclear fractions. We also examined the effects of MBE and delphinidins against rotenone-induced mitochondrial dysfunction. Results Blue light-induced cell death, increased intracellular ROS generation and mitochondrial fragmentation, decreased ATP-production coupled respiration, caused lysosomal membrane permeabilization, and increased ATF4 protein level. Treatment with MBE and its main constituents, delphinidin 3-O-sambubioside-5-O-glucoside and delphinidin 3,5-O-diglucoside, prevented these defects. Furthermore, MBE and delphinidins also protected 661W cells from rotenone-induced cell death. Conclusions Maqui berry may be a useful protective agent for photoreceptors against the oxidative damage induced by exposure to blue light. Graphical abstract