Abstract Title:

Distinct mechanisms underlie distinct polyphenol-induced neuroprotection.

Abstract Source:

J Pharmacol Exp Ther. 2006 Aug;318(2):476-83. Epub 2006 Apr 27. PMID: 17118359

Abstract Author(s):

Keiko Yazawa, Takeshi Kihara, Huilian Shen, Yoshiari Shimmyo, Tetsuhiro Niidome, Hachiro Sugimoto

Article Affiliation:

Department of Neuroscience for Drug Discovery, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto 606-8501, Japan.


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.

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