| 저자(한글) |
Sohn, Eun Jeong,Shin, Min Jea,Kim, Dae Won,Son, Ora,Jo, Hyo Sang,Cho, Su Bin,Park, Jung Hwan,Lee, Chi Hern,Yeo, Eun Ji,Choi, Yeon Joo,Yu, Yeon Hee,Kim, Duk-Soo,Cho, Sung-Woo,Kwon, Oh Shin,Cho, Yong-Ju |
| 초록 |
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 stress-induced 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. |
