Hydroxytyrosol protects retinal pigment epithelial cells from acrolein-induced oxidative stress and mitochondrial dysfunction
文献类型:期刊论文
作者 | Liu, Zhongbo2,3; Sun, Lijuan2; Zhu, Lu2,3; Jia, Xu2; Li, Xuesen2,3; Jia, Haiqun2,3; Wang, Ying4; Weber, Peter4; Long, Jiangang; Liu, Jiankang1 |
刊名 | Journal of neurochemistry
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出版日期 | 2007-12-01 |
卷号 | 103期号:6页码:2690-2700 |
关键词 | Dna damage Hydroxytyrosol Macular degeneration Mitochondrial membrane potential Nuclear factor-e2-related factor 2 Protein carbonyl |
ISSN号 | 0022-3042 |
DOI | 10.1111/j.1471-4159.2007.04954.x |
通讯作者 | Liu, jiankang(j.liu@uci.edu) |
英文摘要 | Hydroxytyrosol (hts) is a natural polyphenol abundant in olive oil. increasing evidence indicates hts has beneficial effect on human health for preventing various diseases. in the present study, we investigated the protective effects of hts on acrolein-induced toxicity in human retinal pigment epithelial cell line, arpe-19, a cellular model of smoking- and age-related macular degeneration. acrolein, a major component of the gas phase cigarette smoke and also a product of lipid peroxidation in vivo, at 75 mu mol/l for 24 h caused significant loss of cell viability, oxidative damage (increase in oxidant generation and oxidative damage to proteins and dna, decrease in antioxidants and antioxidant enzymes, and also inactivation of the keap1/nrf2 pathway), and mitochondrial dysfunction (decrease in membrane potential, activities of mitochondrial complexes, viable mitochondria, oxygen consumption, and factors for mitochondrial biogenesis, and increase in calcium). pre-treatment with hts dose dependently and also time dependently protected the arpe-19 cells from acrolein-induced oxidative damage and mitochondrial dysfunction. a short-term pre-treatment with hts (48 h) required > 75 mu mol/l for showing protection while a long-term pre-treatment (7 days) showed protective effect from 5 mu mol/l on. the protective effect of hts in this model was as potent as that of established mitochondria-targeting antioxidant nutrients. these results suggest that hts is also a mitochondrial-targeting antioxidant nutrient and that dietary administration of hts may be an effective measure in reducing and or preventing cigarette smoke-induced or age-related retinal pigment epithelial degeneration, such as age-associated macular degeneration. |
WOS研究方向 | Biochemistry & Molecular Biology ; Neurosciences & Neurology |
WOS类目 | Biochemistry & Molecular Biology ; Neurosciences |
语种 | 英语 |
WOS记录号 | WOS:000207062600014 |
出版者 | WILEY-BLACKWELL PUBLISHING, INC |
URI标识 | http://www.irgrid.ac.cn/handle/1471x/2381640 |
专题 | 中国科学院大学 |
通讯作者 | Liu, Jiankang |
作者单位 | 1.Univ Calif Irvine, Inst Brain Aging & Dementia, Gillespie Neurosci Res Facil 1261, Irvine, CA 92697 USA 2.Chinese Acad Sci, Inst Nutr Sci, Shanghai Inst Biol Sci, Shanghai, Peoples R China 3.Chinese Acad Sci, Grad Sch, Beijing, Peoples R China 4.R&D Human Nutr & Hlth, DSM Nutr Prod, Basel, Switzerland |
推荐引用方式 GB/T 7714 | Liu, Zhongbo,Sun, Lijuan,Zhu, Lu,et al. Hydroxytyrosol protects retinal pigment epithelial cells from acrolein-induced oxidative stress and mitochondrial dysfunction[J]. Journal of neurochemistry,2007,103(6):2690-2700. |
APA | Liu, Zhongbo.,Sun, Lijuan.,Zhu, Lu.,Jia, Xu.,Li, Xuesen.,...&Liu, Jiankang.(2007).Hydroxytyrosol protects retinal pigment epithelial cells from acrolein-induced oxidative stress and mitochondrial dysfunction.Journal of neurochemistry,103(6),2690-2700. |
MLA | Liu, Zhongbo,et al."Hydroxytyrosol protects retinal pigment epithelial cells from acrolein-induced oxidative stress and mitochondrial dysfunction".Journal of neurochemistry 103.6(2007):2690-2700. |
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来源:中国科学院大学
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