PEP-1-GSTpi protein enhanced hippocampal neuronal cell survival after oxidative damage

BMB Reports

Dae Won Kim^2¹  Min Jea Shin^1²  Ora Son^1³  Eun Jeong Sohn^1⁴  Su Bin Cho^1⁵  Hyo Sang Jo^1⁶ 

[1] Department of Anatomy, College of Medicine, Soonchunhyang University, Cheonan 31538^3;Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangnung-Wonju National University, Gangneung 25457^2;Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505^4;Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chunchon 24252^1;Department of Neurosurgery, Hallym University Medical Center, Chuncheon 24253, Korea^6;School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu 41566^5

关键词: Apoptotic signals;   

DOI  :  

学科分类：生物化学/生物物理

来源: Korean Society for Biochemistry and Molecular Biology

【 摘 要 】

Reactive oxygen species generated under oxidative stress are involved in neuronal diseases, including ischemia. Glutathione S-transferase pi (GSTpi) is a member of the GST family and is known to play important roles in cell survival. We investigated the effect of GSTpi against oxidative stress-induced hippocampal HT-22 cell death, and its effects in an animal model of ischemic injury, using a cell-permeable PEP-1-GSTpi protein. PEP-1-GSTpi was transduced into HT-22 cells and significantly protected against H2O2-treated cell death by reducing the intracellular toxicity and regulating the signal pathways, including MAPK, Akt, Bax, and Bcl-2. PEP-1-GSTpi transduced into the hippocampus in animal brains, and markedly protected against neuronal cell death in an ischemic injury animal model. These results indicate that PEP-1-GSTpi acts as a regulator or an antioxidant to protect against oxidative stressinduced cell death. Our study suggests that PEP-1-GSTpi may have potential as a therapeutic agent for the treatment of ischemia and a variety of oxidative stress-related neuronal diseases.

【 授权许可】

Unknown