Protective Effects of Copper Chaperone for Cu,Zn-SOD (CCS) Against Ischemic Neuronal Damage in theFocal Cerebral Ischemia in Rat

초록

Reactive oxygen species (ROS) contribute to the development of various diseases in humans. Cu,Znsuperoxidedismutase (SOD) is one of major means by which cells counteract the deleterious effects ofROS. SOD activity is dependent upon bound copper ions supplied by its partner metallochaperoneprotein, a copper chaperone for SOD (CCS). In the present study, we investigated the effect of CCSagainst neuronal damage in the rat brain after middle cerebral artery occlusion (MCAO). To elucidate theprotecitve effect of CCS on ischemic damage, we used PEP-1-CCS fusion protein in a cerebral infarctioninduced by MCAO. In the PEP-1-CCS-treated group, the infarct volume stained with triphenyltetrazoliumchloride (TTC) after MCAO was decreased by 67% compared to that in the vehicle-treated group. Thisresult suggests that CCS is essential to activate SOD, and that transduction of PEP-1-CCS provides apotential strategy for therapeutic delivery in various diseases including stroke related to SOD or ROS.

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