期刊
MARINE DRUGS
卷 19, 期 2, 页码 -出版社
MDPI
DOI: 10.3390/md19020114
关键词
fucoxanthin; retinal pigment epithelium; premature senescence; age-related macular degeneration
资金
- Ministry of Science and Technology, Taiwan [MOST 108-2320-B-715-003-]
- Mackay Medical College, Taiwan [1081H03, 1091B05]
- Mackay Memorial Hospital, Taiwan [MMH-MM-10903]
The study demonstrates that fucoxanthin protects RPE cells from oxidative stress-induced premature senescence and decreased photoreceptor cell loss. Fucoxanthin treatment significantly inhibited reactive oxygen species generation and reduced malondialdehyde concentrations in oxidative stress-induced RPE cell damage. Additionally, fucoxanthin may protect against premature senescence and cellular dysfunction in retinal cells exposed to oxidative stress.
Oxidative stress is identified as a major inducer of retinal pigment epithelium (RPE) cell dysregulation and is associated with age-related macular degeneration (AMD). The protection of RPE disorders plays an essential role in the pathological progress of retinal degeneration diseases. The pharmacological functions of fucoxanthin, a characteristic carotenoid, including anti-inflammatory and antioxidant properties, may ameliorate an outstanding bioactivity against premature senescence and cellular dysfunction. This study demonstrates that fucoxanthin protects RPE cells from oxidative stress-induced premature senescence and decreased photoreceptor cell loss in a sodium iodate-induced AMD animal model. Similarly, oxidative stress induced by hydrogen peroxide, nuclear phosphorylated histone (gamma H2AX) deposition and premature senescence-associated beta-galactosidase staining were inhibited by fucoxanthin pretreatment in a human RPE cell line, ARPE-19 cells. Results reveal that fucoxanthin treatment significantly inhibited reactive oxygen species (ROS) generation, reduced malondialdehyde (MDA) concentrations and increased the mitochondrial metabolic rate in oxidative stress-induced RPE cell damage. Moreover, atrophy of apical microvilli was inhibited in cells treated with fucoxanthin after oxidative stress. During aging, the RPE undergoes well-characterized pathological changes, including amyloid beta (A beta) deposition, beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) expression and tight junction disruption, which were also reduced in fucoxanthin-treated groups by immunofluorescence. Altogether, pretreatment with fucoxanthin may protect against premature senescence and cellular dysfunction in retinal cells by oxidative stress in experimental AMD animal and human RPE cell models.
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