| Protective effects of Tat-NQO1 against oxidative stress-induced HT-22 cell damage and ischemic injury in an animal model |
| Soo Young Choi1,*, Hyo Sang Jo1,#, Duk-Soo Kim2,#, Eun Hee Ahn1,#, Dae Won Kim3, Min Jea Shin1, Su Bin Cho1, Jung Hwan Park1, Chi Hern Lee1, Eun Ji Yeo1, Yeon Joo Choi1, Hyeon Ji Yeo1, Christine Seok Young Chung1, Sung-Woo Cho4, Kyu Hyung Han1 |
1Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University,
2Department of Anatomy, College of Medicine, Soonchunhyang University,
33Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, Gangneung-Wonju National University,
4Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine |
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Abstract
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. Therefore, we investigated the effects of cell permeable Tat-NQO1 protein on hippocampal HT-22 cells and in an animal ischemia model. 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 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 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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| Abstract, Accepted Manuscript(in press) [Submitted on July 21, 2016, Accepted on August 24, 2016] |
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