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Published on: September 2, 2010
KN-62 provides neuroprotection against glutamate-induced excitotoxicity in neurons
1Research Center of Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou 221002, China.
Aim:
To study the effects of KN-62, an inhibitor of Ca(2+)-calmodulin dependent protein kinase II (CCDPK II), on the damage of cortical neurons and mechanisms of the loss of CCDPK II activity induced by sodium glutamate (Glu).
Methods:
CCDPK II activity was measured by 32P incorporation and backphosphorylations of endogenous proteins were studied by autoradiography.
Results:
1) KN-62 provided partial protection against excitotoxical damage only before Glu (100 mumol.L-1, 10 min) treatment. 2) KN-62 markedly suppressed the loss of CCDPK II activity induced by Glu from 48.0% to 90.6%. 3) Backphosphorylation of endogenous proteins (especially the 50 kDa protein) reduced to 78.2% of control after treatment with Glu, and the reduction was protected with KN-62 added before Glu.
Conclusion:
KN-62 provided the protection against excitotoxicity and the loss of CCDPK II activity as well as backphosphorylation of endogenous proteins induced by Glu. The neuroprotection provided by KN-62 was due to the inhibition of autophosphorylation of CCDPK II.
