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Delphinidin Ameliorates Beta-Amyloid-Induced Neurotoxicity by Inhibiting Calcium Influx and Tau Hyperphosphorylation

Authors
Kim, Hyo-ShinSul, DonggeunLim, Ji-YounLee, DonghoJoo, Seong SooHwang, Kwang WooPark, So-Young
Issue Date
7월-2009
Publisher
TAYLOR & FRANCIS LTD
Keywords
delphinidin; beta-amyloid; calcium influx; tau hyperphosphorylation; PC12 cells
Citation
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY, v.73, no.7, pp.1685 - 1689
Indexed
SCIE
SCOPUS
Journal Title
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
Volume
73
Number
7
Start Page
1685
End Page
1689
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/119742
DOI
10.1271/bbb.90032
ISSN
0916-8451
Abstract
Beta-amyloid (A beta) has been suggested to induce neurotoxicity in Alzheimer's disease. We evaluated the neuroprotective effects of delphinidin, an anthocyanidin commonly present in pigmented fruits and vegetables, against A beta-induced toxicity. A beta (25-35) significantly decreased the viability of PC12 cells, and this was accompanied by an increase in intracellular calcium levels and tau phosphorylation. However, treatment with delphinidin rescued PC12 cells from A beta by attenuating the elevation of intracellular calcium levels and tau phosphorylation. Taken together, these results suggest that delphinidin protects PC12 cells against A beta-induced toxicity by attenuating intracellular calcium influx and tau hyperphosphorylation.
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