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KN-62 provides neuroprotection against glutamate-induced excitotoxicity in neurons.

  
@article{APS8308,
	author = {Can Gao and Guang-yi Zhang},
	title = {KN-62 provides neuroprotection against glutamate-induced excitotoxicity in neurons.},
	journal = {Acta Pharmacologica Sinica},
	volume = {20},
	number = {11},
	year = {2016},
	keywords = {},
	abstract = {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.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/8308}
}