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( Hyo Sang Jo ),( Duk-soo Kim ),( Eun Hee Ahn ),( Dae Won Kim ),( Min Jea Shin ),( Su Bin Cho ),( Jung Hwan Park ),( Chi Hern Lee ),( Eun Ji Yeo ),( Yeon Joo Choi ),( Hyeon Ji Yeo ),( Christine Seok Y 생화학분자생물학회(구 한국생화학분자생물학회) 2016 BMB Reports Vol.49 No.11
Oxidative stress is closely associated with various diseases and is considered to be a major factor in ischemia. NAD(P)H: quinone oxidoreductase 1 (NQO1) protein is a known antioxidant protein that plays a protective role in various cells against oxidative stress. We therefore investigated the effects of cell permeable Tat-NQO1 protein on hippocampal HT-22 cells, and in an animal ischemia model. The Tat-NQO1 protein transduced into HT-22 cells, and significantly inhibited against hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced cell death and cellular toxicities. Tat-NQO1 protein inhibited the Akt and mitogen activated protein kinases (MAPK) activation as well as caspase-3 expression levels, in H<sub>2</sub>O<sub>2</sub> exposed HT-22 cells. Moreover, Tat-NQO1 protein transduced into the CA1 region of the hippocampus of the animal brain and drastically protected against ischemic injury. Our results indicate that Tat-NQO1 protein exerts protection against neuronal cell death induced by oxidative stress, suggesting that Tat-NQO1 protein may potentially provide a therapeutic agent for neuronal diseases. [BMB Reports 2016; 49(11): 617-622]