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KMID : 0624620160490110617
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BMB Reports
2016 Volume.49 No. 11 p.617 ~ p.622
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Protective effects of Tat-NQO1 against oxidative stress-induced HT-22 cell damage, and ischemic injury in animals
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Jo Hyo-Sang
Kim Duk-Soo
Ahn Eun-Hee
Kim Dae-Won
Shin Min-Jea
Cho Su-Bin
Park Jung-Hwan
Lee Chi-Hern
Yeo Eun-Ji
Choi Yeon-Joo
Yeo Hyeon-Ji
Chung Christine Seok-Young
Cho Sung-Woo
Han Kyu-Hyung
Park Jin-Seu
Eum Won-Sik
Choi Soo-Young
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Abstract
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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 (H2O2)-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 H2O2 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.
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KEYWORD
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Akt/MAPK, Ischemia, Oxidative stress, Protein therapy, Tat-NQO1
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