Anti-Apoptotic Effects of Carotenoids in Neurodegeneration

被引:90
作者
Park, Han-A [1 ]
Hayden, Mary Margaret [1 ]
Bannerman, Sydni [1 ]
Jansen, Joseph [1 ]
Crowe-White, Kristi M. [1 ]
机构
[1] Univ Alabama, Dept Human Nutr & Hospitality Management, Coll Human Environm Sci, Tuscaloosa, AL 35487 USA
关键词
apoptosis; mitochondria; carotenoid; neurodegeneration; antioxidant; TRAUMATIC BRAIN-INJURY; PERMEABILITY TRANSITION PORE; TRANSCRIPTION FACTOR NRF2; DEPRESSIVE-LIKE BEHAVIOR; PROGRAMMED CELL-DEATH; AMYLOID-BETA PEPTIDE; C-SUBUNIT RING; N-BCL-XL; OXIDATIVE STRESS; PARKINSONS-DISEASE;
D O I
10.3390/molecules25153453
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Apoptosis, programmed cell death type I, is a critical part of neurodegeneration in cerebral ischemia, Parkinson's, and Alzheimer's disease. Apoptosis begins with activation of pro-death proteins Bax and Bak, release of cytochrome c and activation of caspases, loss of membrane integrity of intracellular organelles, and ultimately cell death. Approaches that block apoptotic pathways may prevent or delay neurodegenerative processes. Carotenoids are a group of pigments found in fruits, vegetables, and seaweeds that possess antioxidant properties. Over the last several decades, an increasing number of studies have demonstrated a protective role of carotenoids in neurodegenerative disease. In this review, we describe functions of commonly consumed carotenoids including lycopene, beta-carotene, lutein, astaxanthin, and fucoxanthin and their roles in neurodegenerative disease models. We also discuss the underlying cellular mechanisms of carotenoid-mediated neuroprotection, including their antioxidant properties, role as signaling molecules, and as gene regulators that alleviate apoptosis-associated brain cell death.
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页数:19
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