Abstract
BackgroundOxidative damage to retinal pigment epithelial (RPE) cells contributes to the development of age-related macular degeneration, which is among the leading causes of visual loss in elderly people. In the present study, we evaluated the protective role of triphenylphosphonium (TPP)-Niacin against hydrogen peroxide (H2O2)-induced oxidative stress in RPE cells.MethodsThe cellular viability, lactate dehydrogenase release, reactive oxygen species (ROS) generation, and mitochondrial function of retinal ARPE-19 cells were determined under treatment with H2O2 or pre-treatment with TPP-Niacin. The expression level of mitochondrial related genes and some transcription factors were assessed using real-time polymerase chain reaction (RT-qPCR).ResultsTPP-Niacin significantly improved cell viability, reduced ROS generation, and increased the antioxidant enzymes in H2O2-treated ARPE-19 cells. Mitochondrial dysfunction from the H2O2-induced oxidative stress was also considerably diminished by TPP-Niacin treatment, along with reduction of the mitochondrial membrane potential (MMP) and upregulation of the mitochondrial-associated gene. In addition, TPP-Niacin markedly enhanced the expression of transcription factors (PGC-1α and NRF2) and antioxidant-associated genes (especially HO-1 and NQO-1).ConclusionWe verified the protective effect of TPP-Niacin against H2O2-induced oxidative stress in RPE cells. TPP-Niacin is believed to protect against mitochondrial dysfunction by upregulating antioxidant-related genes, such as PGC-1α, NRF2, HO-1, and NQO-1, in RPE cells.
Highlights
Oxidative damage to retinal pigment epithelial (RPE) cells contributes to the development of agerelated macular degeneration, which is among the leading causes of visual loss in elderly people
Cell viability and protective effect of TPP-niacin on ARPE19 cells To evaluate the optimal concentration of TPP-Niacin (Fig. 1a) that can be used without causing cytotoxicity, the ARPE-19 cells were incubated with various concentrations of TPP-Niacin for 24, 48, and 72 h
The protective effects of TPPNiacin were assessed by the lactate dehydrogenase (LDH) assay
Summary
Oxidative damage to retinal pigment epithelial (RPE) cells contributes to the development of agerelated macular degeneration, which is among the leading causes of visual loss in elderly people. Despite being a condition of unknown etiology, oxidative stress is considered as a major influence on RPE cells in AMD pathophysiology [5,6,7]. RPE cells have high metabolic rates with enriched mitochondrial population, and the oxidative phosphorylation process produces adenosine triphosphate (ATP), indicating the generation of high amounts of reactive oxygen species (ROS) [8]. Intramitochondrial oxidative stress is connected with processes ruling cell survival, such as mitochondrial flexibility, apoptosis, and autophagy, in AMD [9]. Protecting RPE cells from oxidative damage is necessary for preventing or weakening AMD
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