Seon Ae Eom, Dae Won Kim, Min Jea Shin, Eun Hee Ahn, Seok Young Chung, Eun Jeong Sohn, Hyo Sang Jo, Su-Jeong Jeon, Duk-Soo Kim, Hyeok Yil Kwon, Sung-Woo Cho, Kyu Hyung Han, Jinseu Park, Won Sik Eum, Soo Young Choi
BMB reports 2015 JulParkinson's disease (PD) is a neurodegenerative disability caused by a decrease of dopaminergic neurons in the substantia nigra (SN). Although the etiology of PD is not clear, oxidative stress is believed to lead to PD. Catalase is antioxidant enzyme which plays an active role in cells as a reactive oxygen species (ROS) scavenger. Thus, we investigated whether PEP-1-Catalase protects against 1-methyl-4-phenylpyridinium (MPP+) induced SH-SY5Y neuronal cell death and in a 1-methyl- 4-phenyl-1,2,3,6-trtrahydropyridine (MPTP) induced PD animal model. PEP-1-Catalase transduced into SH-SY5Y cells significantly protecting them against MPP+-induced death by decreasing ROS and regulating cellular survival signals including Akt, Bax, Bcl-2, and p38. Immunohistochemical analysis showed that transduced PEP-1-Catalase markedly protected against neuronal cell death in the SN in the PD animal model. Our results indicate that PEP-1-Catalase may have potential as a therapeutic agent for PD and other oxidative stress related diseases.
Seon Ae Eom, Dae Won Kim, Min Jea Shin, Eun Hee Ahn, Seok Young Chung, Eun Jeong Sohn, Hyo Sang Jo, Su-Jeong Jeon, Duk-Soo Kim, Hyeok Yil Kwon, Sung-Woo Cho, Kyu Hyung Han, Jinseu Park, Won Sik Eum, Soo Young Choi. Protective effects of PEP-1-Catalase on stress-induced cellular toxicity and MPTP-induced Parkinson's disease. BMB reports. 2015 Jul;48(7):395-400
PMID: 25322954
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