This study aimed to evaluate the effects of lutein (LUT) combined with cyanidin-3-O-glucoside (C3G) on age-related macular degeneration (AMD). Three complementary models were used to investigate the antioxidant effects, including free radical scavenging models, a cell model, and a mouse gavage assay. The results revealed that LUT combined with C3G at molar ratios ranging from 1:2 to 1:5 exhibited synergistic antioxidant effects in vitro. Compared with LUT/C3G alone, LUT:C3G (1:5) increased superoxide dismutase (SOD) and catalase (CAT) activities by 50.22%, 33.73% and 86.21%, 30.77%, respectively, increased glutathione (GSH) levels by 79.31% and 36.82%, and decreased malondialdehyde (MDA) levels by 50.04% and 31.11%. The combination treatment increased the mRNA and protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO1) and decreased the level of Kelch-like ECH-associated protein 1 (Keap1). Furthermore, Nrf2 knockdown in ARPE-19 cells significantly inhibited combination treatment-induced Nrf2 protein expression and nuclear translocation, as well as HO-1 and NQO1 expression. A mouse model of AMD demonstrated that LUT combined with C3G activated the Keap1/Nrf2/HO-1/NQO1 signalling pathway, thereby preventing retinal oxidative stress.

In order to scientifically evaluate the health benefits of nut and dried fruit combinations, the antioxidant capacity of various combination of nuts with dried fruits was evaluated by chemical extraction method, an in vitro digestion model and a mouse model. The results of the chemical extraction method showed that the nut and dried fruit combinations were rich in nutrients such as polyphenols, fatty acids and proteins, and their capacity to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and 2,2’-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) radical cation and ferric reducing antioxidant power (FRAP) were significantly enhanced compared to those of the nuts. The in vitro digestion results showed that the phenolic content of the combinations was increased by 2.90%–60.38% and DPPH and ABTS radical cation scavenging capacity by 1.23%–18.60% compared to that of either alone. The best synergistic antioxidant effect was achieved with a 6:4 mixture of nuts and dried fruits. Meanwhile, the combinations of nuts and dried fruits increased the activity of catalase (CAT), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) in the serum and liver of mice after gastrointestinal digestion, effectively inhibited the production of malondialdehyde (MDA) and preserved the morphological integrity of mouse hepatocytes. In conclusion, the mixture of nuts and dried fruits has a synergistic antioxidant effect and good antioxidant capacity in vitro and in vivo.

In order to improve the bioavailability of lutein (LUT), a novel lutein-stevioside nanoparticle (LUT-STE) were prepared previously, but the information about LUT-STE on protecting of eye health was limited. This study investigated the effect of LUT-STE on antioxidant activity of H₂O₂-induced human retinal pigment epithelial (ARPE) cells. LUT and LUT-STE (final concentration of 5 μg/mL) significantly enhanced cell viability from (74.84 ± 5.10)% to (81.92 ± 10.01)% (LUT) and (89.33 ± 4.34)% (LUT-STE), and inhibited the cell apoptosis (P < 0.05). After pretreatment with LUT-STE in ARPE cells, the levels of superoxide dismutase (SOD), catalase (CAT) and glutathion peroxidase (GSH-Px) in ARPE cells were significantly increased (P < 0.05), the contents of reactive oxygen species (ROS) and malondialdehyde (MDA) were decreased. In addition, the vascular endothelial growth factor (VEGF) levels were inhibited by 13.61% and 17.39%, respectively, pretreatment with LUT and LUT-STE. Western blotting results showed that the pretreatment with LUT-STE inhibited the expression of caspase-9 and caspase-3 and up-regulated Bcl-2/Bax pathway to inhibit H₂O₂-induced apoptosis. In summary, the novel delivery LUT-STE had more pronounced inhibitory effect on H₂O₂-induced damage in human ARPE cells.