Neuroprotective effects of anthocyanin- and proanthocyanidin-rich extracts in cellular models of Parkinson’s disease. Brain Research. February 2014. Epub ahead of print. Katherine E. Strathearn, Gad G. Yousef, Mary H. Grace, Susan L. Roy, Mitali A. Tambe, Mario G. Ferruzzi, Qing-Li Wu, James E. Simon, Mary Ann Lila and Jean-Christophe Rochet.
Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University; Departments of Food Science and Foods and Nutrition, Purdue University; Department of Plant Biology & Pathology, Rutgers University; Plants for Human Health Institute, Department of Food Bioprocessing and Nutrition Sciences, North Carolina State University, Nc Research Campus.
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.
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