Journal
BRAIN RESEARCH
Volume 1555, Issue -, Pages 60-77Publisher
ELSEVIER
DOI: 10.1016/j.brainres.2014.01.047
Keywords
Anthocyanin; Microglial activation; Mitochondria; Parkinson's disease; Proanthocyanidin; Rotenone
Categories
Funding
- NIH [RO3 AG027123, R21 AG039718]
- Pilot Grant from the Purdue-UAB Botanicals Research Center [NIH P50 AT000477-06]
- Collaboration in Biomedical Research Grant from Purdue University and Indiana University School of Medicine [CBR4]
- Showalter Trust
- Research Facilities Improvement Program from the National Center for Research Resources of the NIH [C06-14499, C06-15480]
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Neuropathological evidence indicates that dopaminergic cell death in Parkinson's disease (PD) involves impairment of mitochondrial complex I, oxidative stress, microglial activation, and the formation of Lewy bodies. Epidemiological findings suggest that the consumption of berries rich in anthocyanins and proanthocyanidins may reduce PD risk. In this study, we investigated whether extracts rich in anthocyanins, proanthocyanidins, or other polyphenols suppress the neurotoxic effects of rotenone in a primary cell culture model of PD. Dopaminergic cell death elicited by rotenone was suppressed by extracts prepared from blueberries, grape seed, hibiscus, blackcurrant, and Chinese mulberry. Extracts rich in anthocyanins and proanthocyanidins exhibited greater neuroprotective activity than extracts rich in other polyphenols, and a number of individual anthocyanins interfered with rotenone neurotoxicity. The blueberry and grape seed extracts rescued rotenone-induced defects in mitochondrial respiration in a dopaminergic cell line, and a purple basal extract attenuated nitrite release from microglial cells stimulated by lipopolysaccharide. These findings suggest that anthocyanin- and proanthocyanidin-rich botanical extracts may alleviate neurodegeneration in PD via enhancement of mitochondrial function. (C) 2014 Elsevier B.V. All rights reserved.
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