Excessive exposure to blue light caused by the wide use of smart phones, tablet computers and other electronic devices can induce retinal photooxidative damage, causing a public health problem that cannot be overlooked. Anthocyanins, edible plant pigments, are widely distributed in dark-colored vegetables, berries and cereals. The individual daily intake of anthocyanins has been estimated to be tens of milligrams per person. Previous studies have reported that anthocyanins exert protective effects on retinal cells and are beneficial for vision health, but the specific mechanism of action is not yet clear. In this paper, we review the current status of research on the absorption and metabolism of anthocyanins, the mechanism of light-induced retinal oxidative damage and the mechanism by which anthocyanins protect the retina from light-induced damage, focusing on the fact that anthocyanins protect against photo-oxidation and photo-degradation of bisretinoids, reduce damage caused by lipid peroxidation products, activate antioxidant pathways, reduce inflammation, suppress endoplasmic reticulum stress, and inhibit cells apoptosis. Furthermore, we systematically elucidate the key targets for the protective effect of anthocyanins on retinal cells, which provide scientific evidence for anthocyanins as functional food factors to maintain vision health.

Objective: To investigate the effect of cyanidin-3-O-glucoside (C3G) on brain damage and gut microbiota in naturally aging mice. Methods: Mice aged 2 and 18 months were divided into four groups: young control, young + C3G, aging model and aged + C3G. The second and fourth groups were administered by gavage with 50 mg/kg C3G consecutively for eight weeks. The following parameters were assessed: serum levels of inflammatory factors and antioxidant indexes, expression levels of neurotrophic factors and brain damage markers in brain tissue; microbial diversity and metabolite changes in intestinal contents. Results: C3G significantly decreased the level of inflammatory factors (P < 0.05), increased the activity of antioxidant enzymes (P < 0.05), and up-regulated the expression of brain-derived neurotrophic factor (BDNF), while inhibiting the production of brain damage markers including beta amyloid 1-42 (Aβ_1-42) (P < 0.05). In addition, C3G increased the relative abundance of Faecalibaculum and Bifidobacterium in the gut, while decreasing the level of Enterorhabdus. These changes in gut microbiota contributed to the production of docosahexaenoic acid and eicosapentaenoic acid and decreased linoleic acid levels (P < 0.05). Correlation analysis showed that Faecalibaculum and Bifidobacterium were negatively correlated with inflammatory factors and nerve damage indicators, but positively correlated with antioxidant capacity and neurotrophic factors. Conclusion: C3G can alleviate aging-related neurological damage and improve brain health in naturally aging mice by modulating gut microbiota. This finding may provide a theoretical basis for the development of aging-delaying health foods containing anthocyanins.

Cyanidin-3-glucoside (C3G) is the most common anthocyanin in dark grains and berries and is a food functional factor to improve visual health. However, the mechanisms of C3G on blue light-induced retinal pigment epithelial (RPE) cell photooxidative damage needs further exploration. We investigated the effects of C3G on blue light-irradiated A2E-containing RPE cells and explored whether sphingolipid, mitogen-activated protein kinase (MAPK), and mitochondria-mediated pathways are involved in this mechanism. Blue light irradiation led to mitochondria and lysosome damage in RPE cells, whereas C3G preserved mitochondrial morphology and function and maintained the lysosomal integrity. C3G suppressed the phosphorylation of JNK and p38 MAPK and mitochondria-mediated pathways to inhibit RPE cell apoptosis. Lipidomics data showed that C3G protected RPE cells against blue light-induced lipid peroxidation and apoptosis by maintaining sphingolipids balance. C3G significantly inhibited ceramide (Cer d18:0/15:0, Cer d18:0/16:0 and Cer d18:0/18:0) accumulation and elevated galactosylceramide (GalCer d18:1/15:0 and GalCer d18:1/16:0) levels in the irradiated A2E-containing RPE cells. Furthermore, C3G attenuated cell membrane damage by increasing phosphatidylcholine and phosphatidylserine levels. C3G inhibited apoptosis and preserved the structure of mitochondria and lysosome by regulating sphingolipid signaling and suppression of MAPK activation in RPE cells. Thus, dietary supplementation of C3G prevents retinal photooxidative damage.