Lutein and Zeaxanthin Isomers Protect against Light-Induced Retinopathy via Decreasing Oxidative and Endoplasmic Reticulum Stress in BALB/cJ Mice
1
Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
2
Department of Ophthalmology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH 44195, USA
3
Department of Clinical Medicine, Faculty of Aerospace Medicine, Key Laboratory of Aerospace Medicine of the National Education Ministry, Fourth Military University, Xi’an 710032, China
4
Louis Stokes Cleveland Veterans Affairs Medical Center, Cleveland, OH 44195, USA
*
Author to whom correspondence should be addressed.
Nutrients 2018, 10(7), 842; https://doi.org/10.3390/nu10070842
Received: 14 May 2018
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Revised: 4 June 2018
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Accepted: 22 June 2018
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Published: 28 June 2018
(This article belongs to the Special Issue Nutrition and Eye Health)
Oxidative stress (OS) and endoplasmic reticulum stress (ERS) are the major factors underlying photoreceptor degeneration. Lutein, RR-zeaxanthin (3R,3’R-zeaxanthin) and RS (meso)-zeaxanthin (3R,3’S-RS- zeaxanthin) (L/Zi) could protect against cell damage by ameliorating OS in retina. In this study, we examined the effect of L/Zi supplementation in a mouse model of photoreceptor degeneration and investigated whether the treatment of L/Zi ameliorated OS and ERS. BALB/cJ mice after light exposure were used as the animal model. The protective effects of L/Zi were observed by electroretinography (ERG) and terminal deoxyuridine triphosphate nick-end labeling (TUNEL) analysis. The underlying mechanisms related to OS and ERS were explored by Western blotting. After L/Zi treatment, the ERG amplitudes were significantly higher, and the number of TUNEL-positive cells was significantly reduced compared to that of the vehicle group. Western blotting results revealed that OS was ameliorated according to the significant downregulation of phosphorylated c-Jun N-terminal kinase (p-JNK), and significant upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2). In addition, ERS was reduced according to the significant downregulation of 78 kDa glucose-regulated protein (GRP78), phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (p-PERK), activating transcription factor 4 (ATF4) and activating transcription factor (ATF6). Our data shows that L/Zi provided functional and morphological preservation of photoreceptors against light damage, which is probably related to its mitigation of oxidative and endoplasmic reticulum stress.
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Keywords:
lutein; RR-zeaxanthin; mesozeaxanthin (RS zeaxanthin); light damage; photoreceptor degeneration; oxidative stress; endoplasmic reticulum stress; electroretinography
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MDPI and ACS Style
Yu, M.; Yan, W.; Beight, C. Lutein and Zeaxanthin Isomers Protect against Light-Induced Retinopathy via Decreasing Oxidative and Endoplasmic Reticulum Stress in BALB/cJ Mice. Nutrients 2018, 10, 842. https://doi.org/10.3390/nu10070842
AMA Style
Yu M, Yan W, Beight C. Lutein and Zeaxanthin Isomers Protect against Light-Induced Retinopathy via Decreasing Oxidative and Endoplasmic Reticulum Stress in BALB/cJ Mice. Nutrients. 2018; 10(7):842. https://doi.org/10.3390/nu10070842
Chicago/Turabian StyleYu, Minzhong, Weiming Yan, and Craig Beight. 2018. "Lutein and Zeaxanthin Isomers Protect against Light-Induced Retinopathy via Decreasing Oxidative and Endoplasmic Reticulum Stress in BALB/cJ Mice" Nutrients 10, no. 7: 842. https://doi.org/10.3390/nu10070842
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