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Distinct mechanisms underlie distinct polyphenol‐induced neuroprotection
Author(s) -
Yazawa Keiko,
Kihara Takeshi,
Shen Huilian,
Shimmyo Yoshiari,
Niidome Tetsuhiro,
Sugimoto Hachiro
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.11.011
Subject(s) - excitotoxicity , glutamate receptor , neuroprotection , chemistry , curcumin , biochemistry , microbiology and biotechnology , nmda receptor , pharmacology , receptor , biology
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.