Ultraviolet radiation, especially UVA, can penetrate the lens, reach the retina, and induce oxidative stress to retinal pigment epithelial (RPE) cells. Even though it is weakly absorbed by protein and DNA, it may trigger the production of reactive oxygen species (ROS) and generate oxidative injury; oxidative injury to the retinal pigment epithelium has been implicated to play a contributory role in age-related macular degeneration (AMD). Studies showed that resveratrol, an abundant and active component of red grapes, can protect several cell types from oxidative stress. In this study, adult RPE cells being treated with different concentrations of resveratrol were used to evaluate the protective effect of resveratrol on RPE cells against UVA-induced damage. Cell viability assay showed that resveratrol reduced the UVA-induced decrease in RPE cell viability. Through flow cytometry analysis, we found that the generation of intracellular H₂O₂ induced by UVA irradiation in RPE cells could be suppressed by resveratrol in a concentration-dependent manner. Results of Western blot analysis demonstrated that resveratrol lowered the activation of UVA-induced extracellular signal-regulated kinase, c-jun-NH₂ terminal kinase and p38 kinase in RPE cells. In addition, there was also a reduction in UVA-induced cyclooxygenase-2 (COX-2) expression in RPE cells pretreated with resveratrol. Our observations suggest that resveratrol is effective in preventing RPE cells from being damaged by UVA radiation, and is worth considering for further development as a chemoprotective agent for the prevention of early AMD.

During the course of proliferative vitreoretinopathy (PVR), the retinal pigment epithelium (RPE) cells will de-differentiate, proliferate, and migrate onto the surfaces of the sensory retina. Several studies have shown that platelet-derived growth factor (PDGF) can induce migration of RPE cells via an Akt-related pathway. In this study, the effect of lutein on PDGF-BB-induced RPE cells migration was examined using transwell migration assays and Western blot analyses. We found that both phosphorylation of Akt and mitochondrial translocation of Akt in RPE cells induced by PDGF-BB stimulation were suppressed by lutein. Furthermore, the increased migration observed in RPE cells with overexpressed mitochondrial Akt could also be suppressed by lutein. Our results demonstrate that lutein can inhibit PDGF-BB induced RPE cells migration through the inhibition of both cytoplasmic and mitochondrial Akt activation.

Background: Urinary incontinence (UI) and poor sleep negatively affect health-related quality of life (HRQoL). This study explored the UI-related factors and the relationships between UI, sleep quality, and HRQoL. Methods: This cross-sectional study collected data from 237 women with type 2 diabetes. Multivariate logistic regression was conducted to identify the factors associated with UI. One-way analysis of variance was used to compare the mean sleep quality and HRQoL scores of women without UI and those who experienced UI of varying severities. Correlation coefficients were estimated, and multivariate linear regression was conducted to examine the relationships between UI severity, sleep quality, and HRQoL. Results: Of the 237 women, 115 (48.52%) experienced UI and 139 (58.65%) were poor sleepers. The three factors associated with UI were advanced age, a higher body mass index, and a history of vaginal delivery. Significant associations between UI severity and sleep quality and between sleep quality and HRQoL were revealed. UI severity and night-time voiding frequency were both associated with sleep quality. Conclusions: One factor associated with UI (body mass index) is modifiable. UI severity is associated with sleep quality as the possible influence of night-time voiding frequency on sleep quality has been considered.