Vitamin D alleviation of oxidative stress in human retinal pigment epithelial cells

Oxidative stress-induced retinal pigment epithelium (RPE) cell damage is a major factor in age-related macular degeneration (AMD). Vitamin D₃ (VD₃) is a powerful antioxidant and it has been suggested to have anti-aging properties and potential for treating AMD. This study aimed to investigate the effect of VD₃ on RPE cell oxidative apoptosis of RPE cells in order to provide experimental evidence for the treatment of AMD.

Human retinal pigment epithelial cell 19 (ARPE-19) cells were divided into four groups: blank group (untreated), model group (incubated in medium with 400 μmol/L H₂O₂ for 1 h), VD₃ group (incubated in medium with 100 μmol/L VD₃ for 24 h), and treatment group (incubated in medium with 400 μmol/L H₂O₂ for 1 h and 100 μmol/L VD₃ for 24 h). Cell viability, cell senescence, ROS content, expression levels of vitamin D specific receptors, Akt, Sirt1, NAMPT, and JNK mRNA expression levels, SOD activity, and MDA, GSH, and GPX levels were measured.

We first established an ARPE-19 cell stress model with H₂O₂. Our control experiment showed that VD₃ treatment had no significant effect on ARPE-19 cell viability within 6–48 h. Treating the stressed ARPE-19 cells with VD₃ showed mixed results; caspase-3 expression was decreased, Bcl-2 expression was increased, MDA level of ARPE-19 cells was decreased, GSH-PX, GPX and SOD levels were increased, the relative mRNA expression levels of Akt, Sirt1, NAMPT were increased (P < 0.05), and the relative mRNA expression level of JNK was decreased (P < 0.05).

VD₃ can potentially slow the development of AMD.