BlingLife ® -Marigold Extract Alleviates Blue Light-Induced Retinal Mitochondria Oxidative Stress and Senescence by Activating NRF2/HO-1 Signaling
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Blue light poses a risk of retinal damage with excessive exposure. BlingLife®-marigold extract (BLM) is an alcohol extract of magrigold, which contains abundant lutein, zeaxanthin and meso-zeaxanthin. This study aimed to explore the role and potential mechanisms of BLM in blue light-induced retinal damage both in vivo and in vitro. Rats or human retinal pigment epithelial cell line (ARPE-19) were exposed to blue LED light with or without BLM treatment. The retinal morphology changes of rat were evaluated by H&E staining. Mitochondrial morphology was examined by using a transmission electron microscope. Besides, mitochondria oxidative stress was evaluated by detecting mitochondrial membrane potential, ROS, MDA and SOD levels. By measuring γH2AX expression and performing SA-β-galactosidase (gal) staining, cell senescence was assessed. Additionally, cell cycle was detected using flow cytometry. Western blot was employed to examine the expression of NRF2 and HO-1. Results indicated that BLM could protect against blue light-induced damage of rat retinal tissues and ARPE-19 cells, as evidenced by the improved histopathological changes, alleviated mitochondria oxidative stress and attenuated senescence of tissues and cells. More importantly, BLM activated NRF2/HO-1 signaling, and addition of NRF2 inhibitor ML385 significantly blocked the protective effects of BLM on ARPE-19 cells exposed to blue light. In conclusion, BLM can provide an effective protection against blue light-induced retinal damage at least partly by activating NRF2/HO-1 signaling, suggesting that BLM may be useful for the prevention of blue light-induced retinal injury
Abstract
Blue light poses a risk of retinal damage with excessive exposure. BlingLife®-marigold extract (BLM) is an alcohol extract of magrigold, which contains abundant lutein, zeaxanthin and meso-zeaxanthin. This study aimed to explore the role and potential mechanisms of BLM in blue light-induced retinal damage both in vivo and in vitro. Rats or human retinal pigment epithelial cell line (ARPE-19) were exposed to blue LED light with or without BLM treatment. The retinal morphology changes of rat were evaluated by H&E staining. Mitochondrial morphology was examined by using a transmission electron microscope. Besides, mitochondria oxidative stress was evaluated by detecting mitochondrial membrane potential, ROS, MDA and SOD levels. By measuring γH2AX expression and performing SA-β-galactosidase (gal) staining, cell senescence was assessed. Additionally, cell cycle was detected using flow cytometry. Western blot was employed to examine the expression of NRF2 and HO-1. Results indicated that BLM could protect against blue light-induced damage of rat retinal tissues and ARPE-19 cells, as evidenced by the improved histopathological changes, alleviated mitochondria oxidative stress and attenuated senescence of tissues and cells. More importantly, BLM activated NRF2/HO-1 signaling, and addition of NRF2 inhibitor ML385 significantly blocked the protective effects of BLM on ARPE-19 cells exposed to blue light. In conclusion, BLM can provide an effective protection against blue light-induced retinal damage at least partly by activating NRF2/HO-1 signaling, suggesting that BLM may be useful for the prevention of blue light-induced retinal injury