Abstract
Aims: The progressive accumulation of beta-amyloid peptide (Aβ), in the form of senile plaques, has been recognized as one of the major causes of Alzheimer's disease (AD) pathology. Increased production of Aβ and the aggregation of Aβ to oligomers have been reported to trigger neurotoxicity, oxidative damage and inflammation. Furthermore, Aβ-induced tau hyperphosphorylation and neurotoxicity are downstream of Aβ. Therefore, we studied the possible neuroprotective effects of caffeic acid against Aβ-induced toxicity. Main methods: Treatment of PC12 cells with 10 μM Aβ (25-35) for 24 h significantly decreased the cell viability; this was accompanied by an increase in intracellular calcium levels and tau phosphorylation with GSK-3β (glycogen synthase kinase-3β) activation (phosphorylation). Key findings: However, pretreatment of the PC12 cells with 10 and 20 μg/ml of caffeic acid, for 1 h prior to Aβ, significantly reversed the Aβ-induced neurotoxicity by attenuating the elevation of intracellular calcium levels and tau phosphorylation. Significance: Taken together, these results suggest that caffeic acid protected the PC12 cells against Aβ-induced toxicity. In addition, the neuroprotective mechanisms of caffeic acid against Aβ attenuated intracellular calcium influx and decreased tau phosphorylation by the reduction of GSK-3β activation.
Original language | English |
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Pages (from-to) | 257-262 |
Number of pages | 6 |
Journal | Life Sciences |
Volume | 84 |
Issue number | 9-10 |
DOIs | |
Publication status | Published - 2009 Feb 27 |
Bibliographical note
Funding Information:This research was supported by the Grant of Medical Research Center for Environmental Toxico-Genomics and Proteomics, funded by Korea Science and Engineering Foundations and Ministry of Science and Technology.
Keywords
- Antioxidant
- Beta-amyloid
- Caffeic acid
- Calcium influx
- GSK-3β
- Tau phosphorylation
ASJC Scopus subject areas
- General Pharmacology, Toxicology and Pharmaceutics
- General Biochemistry,Genetics and Molecular Biology