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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 9015765, 12 pages
https://doi.org/10.1155/2018/9015765
Research Article

Protective Effect of Melatonin against Oxidative Stress-Induced Apoptosis and Enhanced Autophagy in Human Retinal Pigment Epithelium Cells

1School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan
2PhD Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei, Taiwan
3Department of Ophthalmology, Yangming Branch, Taipei City Hospital, Taipei, Taiwan
4Department of Optometry, University of Kang Ning, Taipei, Taiwan
5Department of Health and Welfare, College of City Management, University of Taipei, Taipei, Taiwan
6Graduate Institute of Metabolism and Obesity Sciences, Taipei Medical University, Taipei, Taiwan
7School of Food and Safety, Taipei Medical University, Taipei, Taiwan
8Nutrition Research Center, Taipei Medical University Hospital, Taipei, Taiwan

Correspondence should be addressed to Shih-Min Hsia; wt.ude.umt@aishnayrb

Received 14 March 2018; Revised 1 June 2018; Accepted 6 June 2018; Published 5 August 2018

Academic Editor: Mohamed M. Abdel-Daim

Copyright © 2018 Chih-Chao Chang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Age-related macular degeneration (AMD) affects the retinal macula and results in loss of vision, and AMD is the primary cause of blindness and severe visual impairment among elderly people worldwide. AMD is characterized by the accumulation of drusen in the Bruch’s membrane and dysfunction of retinal pigment epithelial (RPE) cells and photoreceptors. The pathogenesis of AMD remains unclear, and no effective treatment exists. Accumulating evidence indicates that oxidative stress plays a critical role in RPE cell degeneration and AMD. Melatonin is an antioxidant that scavenges free radicals, and it has anti-inflammatory, antitumor, and antiangiogenic effects. This study investigated the antioxidative, antiapoptotic, and autophagic effects of melatonin on oxidative damage to RPE cells. We used hydrogen peroxide (H2O2) to stimulate reactive oxygen species production to cause cell apoptosis in ARPE-19 cell lines. Our findings revealed that treatment with melatonin significantly inhibited H2O2-induced RPE cell damage, decreased the apoptotic rate, increased the mitochondrial membrane potential, and increased the autophagy effect. Furthermore, melatonin reduced the Bax/Bcl-2 ratio and the expression levels of the apoptosis-associated proteins cytochrome c and caspase 7. Additionally, melatonin upregulated the expression of the autophagy-related proteins LC3-II and Beclin-1 and downregulated the expression of p62. Thus, melatonin’s effects on autophagy and apoptosis can protect against H2O2-induced oxidative damage in human RPE cells. Melatonin may have multiple protective effects on human RPE cells against H2O2-induced oxidative damage.