Distinct Mechanisms Underlie Distinct Polyphenol-induced Neuroprotection.
From: Department of Neuroscience for Drug Discovery, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto 606-8501, Japan.
FEBS letters
- Publish Date: Dec 2006
- ISSN: 0014-5793
- Volume: 580
- Issue: 28-29
- Pages: 6623-8
- Medium: Print
- Language: English
- Citation (JAMA): Yazawa Keiko, Kihara Takeshi, Shen Huilian, et al. Distinct Mechanisms Underlie Distinct Polyphenol-induced Neuroprotection.. FEBS Lett. Dec 2006;580:6623-8
Abstract
Glutamate excitotoxicity is mediated by intracellular Ca(2+) overload, caspase-3 activation, and ROS generation. Here, we show that curcumin, tannic acid (TA) and (+)-catechin hydrate (CA) all inhibited glutamate-induced excitotoxicity. Curcumin inhibited PKC activity, and subsequent phosphorylation of NR1 of the NMDA receptor. As a result, glutamate-mediated Ca(2+) influx was reduced. TA attenuated glutamate-mediated Ca(2+) influx only when simultaneously administered, directly interfering with Ca(2+). Both curcumin and TA inhibited glutamate-induced caspase-3 activation. Although Ca(2+) influx was not attenuated by CA, caspase-3 was reduced by direct inhibition of the enzyme. All polyphenols reduced glutamate-induced generation of ROS.
Mesh Headings (Keywords): Animals, Caspase 3, Catechin, Cell Death, Cells, Cultured, Curcumin, Enzyme Activation, Flavonoids, Glutamic Acid, Neurons, Neuroprotective Agents, Neurotoxins, Phenols, Phosphorylation, Protein Kinase C, Rats, Reactive Oxygen Species, Receptors, N-Methyl-D-Aspartate, Tannins
Check for Full Text / PubMed Unique Identifier (PMID): 17118359
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