Lutein suppresses hyperglycemia‐induced premature senescence of retinal pigment epithelial cells by upregulating SIRT1
2018
Hwang, Jung Seok | Han, Sung Gu | Lee, Chi‐Ho | Seo, Han Geuk
Hyperglycemia contributes to the pathogenesis of diabetic complications, such as diabetic retinopathy, by affecting cellular redox state. In this study, we investigated the effects of lutein on hyperglycemia‐induced premature senescence in retinal pigment epithelium (RPE) cells. In ARPE‐19 cells, a spontaneously immortalized cell line derived from human RPE, lutein treatment significantly inhibited high glucose‐triggered premature senescence and production of reactive oxygen species (ROS). Notably, lutein treatment increased SIRT1 mRNA and protein levels, suggesting that lutein exerted its beneficial effects in these cells by upregulating SIRT1 expression. Resveratrol, an activator of SIRT1, mimicked the inhibitory effects of lutein on high glucose‐induced premature senescence and ROS generation, whereas sirtinol, a specific inhibitor of SIRT1, blocked these effects of lutein. Collectively, these observations indicate that lutein interferes with hyperglycemia‐induced RPE senescence by modulating SIRT1 signaling. PRACTICAL APPLICATIONS: Lutein, a xanthophyll carotenoid present in green leafy vegetables and eggs, has been consumed as a dietary supplement to improve eye health. Lutein exhibited anti‐senescent properties by suppressing ROS generation through SIRT1 upregulation in RPE cells exposed to hyperglycemia mimicking diabetic conditions. Thus, we propose that lutein could be applied to therapeutic interventions aimed at treating hyperglycemia‐induced retinal disorders.
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