Page 12 - Q. Neuroscience

[Q. Neuroscience-7]

Neuroprotection of PEP-1-GSTA2 against oxidative stress-

induced ischemic injury

Yeon Joo Choi¹, Hyeon Ji Yeo¹, Eun Ji Yeo¹, Min Jea Shin¹, Dae Won Kim², Jinseu Park¹, Kyu Hyung Han¹,
Keun Wook Lee¹, Jong Kook Park¹, Sung-Woo Cho³, Duk-Soo Kim⁴, Won Sik Eum¹, Soo Young Choi¹

¹Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University,

Chuncheon 24252, Korea, ²Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences,
College of De, Gangneung-Wonju National University, Gangneung 25457, Korea, ³Department of Biochemistry and
Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, Korea, ⁴Department of Anatomy, College

of Medicine, Soonchunhyang University, Cheonan-Si 31538, Korea

Oxidative stress is one of major factors in the pathophysiology of neuronal disease including ischemia. It is well

known that Glutathione S-transferase alpha 2 (GSTA2) has anti-oxidative properties and highly associated with cell
survival by inhibition of oxidative stress. Therefore, we investigated whether GSTA2 protein showed the anti-oxidant

effect in neuronal cells and ischemia animal model. To elucidate the protective mechanism of GSTA2 protein on
ischemic injury, we prepared cell permeable PEP-1-GSTA2 protein and investigated the effects of PEP-1-GSTA2 on

HT-22 cells and in an ischemia animal model. Transduced PEP-1-GSTA2 markedly protected cell death by inhibition
of ROS generation in H2O2-exposed HT-22 cells and this fusion protein modulated the mitogen-activate protein

kinases (MAPKs) and apoptotic signaling pathways. Furthermore, PEP-1-GSTA2 transduced into the brain tissues
and significantly protected hippocampal neuronal cell death in an ischemic animal model. In conclusion, this study

provided crucial evidence that PEP-1-GSTA2 may be potential novel strategy for the treatment of ischemic injury.